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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
\n\n\n\n\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"7004",leadTitle:null,fullTitle:"Metabolomics - New Insights into Biology and Medicine",title:"Metabolomics",subtitle:"New Insights into Biology and Medicine",reviewType:"peer-reviewed",abstract:"This book is mainly for researchers interested in the new developments and applications of metabolomics. It is also important for physicians using metabolomic approaches in the diagnosis of diseases or treatment, and for postgraduate students starting their research projects on metabolomics. The book is divided into two sections as indicated from its title, namely: new insights into biology and new insights into medicine. It gives examples of the different applications of metabolomics from the production of biosurfactants by marine microorganisms to the applications of data from fecal metabolomics, serum metabolomics, and metabolomics of microbiota, as well as the use of Chinese medicines for cancer treatment. Overall, this is a well-written book, containing some very interesting research avenues and cutting-edge approaches. Finally, the editing of this book was of special interest to me and I hope that readers will also find it stimulating.",isbn:"978-1-78985-128-1",printIsbn:"978-1-78985-127-4",pdfIsbn:"978-1-83962-298-4",doi:"10.5772/intechopen.73760",price:119,priceEur:129,priceUsd:155,slug:"metabolomics-new-insights-into-biology-and-medicine",numberOfPages:112,isOpenForSubmission:!1,isInWos:1,isInBkci:!1,hash:"35a30d8241442b716a4aab830b6de28f",bookSignature:"Wael N. Hozzein",publishedDate:"July 1st 2020",coverURL:"https://cdn.intechopen.com/books/images_new/7004.jpg",numberOfDownloads:4178,numberOfWosCitations:3,numberOfCrossrefCitations:11,numberOfCrossrefCitationsByBook:1,numberOfDimensionsCitations:15,numberOfDimensionsCitationsByBook:2,hasAltmetrics:1,numberOfTotalCitations:29,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"January 10th 2018",dateEndSecondStepPublish:"January 31st 2019",dateEndThirdStepPublish:"April 1st 2019",dateEndFourthStepPublish:"June 20th 2019",dateEndFifthStepPublish:"August 19th 2019",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"189233",title:"Prof.",name:"Wael N.",middleName:"Nabil",surname:"Hozzein",slug:"wael-n.-hozzein",fullName:"Wael N. Hozzein",profilePictureURL:"https://mts.intechopen.com/storage/users/189233/images/system/189233.jpeg",biography:"Prof. Wael N. Hozzein is a Professor of Microbiology at the Faculty of Science, Beni-Suef University, Egypt. He received his Ph.D. from Cairo University, Egypt, and went on to work as a visiting scientist at Newcastle University, UK, and Michigan State University, USA. He is the chair professor of the Bioproducts Research Chair at King Saud University, Saudi Arabia. He has vast experience in bacterial taxonomy, microbial biodiversity, and biotechnological applications of bacteria. Prof. Hozzein is the author of more than 180 publications and a guest editor, editorial board member, and reviewer for several international journals. Recently, he was included in Stanford University’s list of the top 2% most-cited scientists. He has been the principal investigator for several funded grants and has also received several awards, including the State Encouragement Prize in Biological Sciences in 2015. Prof. Hozzein has been involved in many academic activities and educational reform projects and initiatives. Recently, he served as an advisor for Nahda University President for Development, Research, and Quality.",institutionString:"Beni-Suef University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"3",totalChapterViews:"0",totalEditedBooks:"3",institution:{name:"Beni-Suef University",institutionURL:null,country:{name:"Egypt"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"43",title:"Biochemistry",slug:"biochemistry-genetics-and-molecular-biology-biochemistry"}],chapters:[{id:"63261",title:"Biosurfactants from Marine Microorganisms",doi:"10.5772/intechopen.80493",slug:"biosurfactants-from-marine-microorganisms",totalDownloads:1156,totalCrossrefCites:3,totalDimensionsCites:6,hasAltmetrics:0,abstract:"The marine biosphere represents a yet underexploited natural source of bioactive compounds, mainly of microbial origin. Among them, biosurfactants (BSs) are functional molecules, which are attracting a great interest due to their biocompatibility, versatility, and applications in several biotechnological fields. BSs are surface active amphipathic compounds, containing both a hydrophilic and a hydrophobic moiety, which are grouped in low (glycolipids and lipopeptides) or high molecular weight (polymeric complexes) compounds. A number of environmental factors such as pH, salinity, temperature, and nutrient availability can affect microbial BS production. Marine microorganisms with different phylogenetic affiliations and isolated from several marine habitats (e.g., seawater, sediments, and higher organisms) worldwide (spanning from the Mediterranean Sea to Antarctica) have been reported as surfactant producers. However, most of the marine microbial world remains still unexplored. The present chapter aims at giving a general overview on the recent advances about BSs of marine origin, in order to enhance the knowledge inherent their production, chemical characterization and identification, interesting biological properties, and potential biotechnological applications.",signatures:"Rosanna Floris, Carmen Rizzo and Angelina Lo Giudice",downloadPdfUrl:"/chapter/pdf-download/63261",previewPdfUrl:"/chapter/pdf-preview/63261",authors:[null],corrections:null},{id:"69917",title:"Fecal Metabolomics Insights of Agavins Intake in Overweight Mice",doi:"10.5772/intechopen.89844",slug:"fecal-metabolomics-insights-of-agavins-intake-in-overweight-mice",totalDownloads:717,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Targeted and non-targeted metabolite profiling can identify biomarkers after a dietary treatment leading to a better understanding of interactions between diet and health. This study was conducted to establish enriched or depleted metabolites in the feces of overweight mice after a diet shift plus agavins or inulins supplementation, and their possible association with beneficial effects on host health. Thirty-eight male C57BL/6 mice were fed with a high-fat diet for 5 weeks followed by a diet shift to a standard diet supplemented with agavins (HF-ST + A) or inulins (HF-ST + I) for five more weeks. Feces were collected before and after prebiotic supplementation for metabolomics analyses. HF-ST + I group increased the fecal excretion of two methyl esters: linoleic and oleic acid, while HF-ST + A mice showed a substantial augment of 2-decenal, fructose, cyclohexanol, and the acids: 10-undecenoic, 3-phenyllactic, nicotinic, 5-hydroxyvaleric, and lactic. From the metabolites identified in HF-ST + A, only lactic acid has been reported previously and associated with beneficial effects on host health. However, the identification of new metabolites, coming from the microbial fermentation of agavins, opens opportunities to transform this information into practical solutions to tackle overweight and associated metabolic syndrome.",signatures:"Alicia Huazano-García, Horacio Claudio Morales-Torres, Juan Vázquez-Martínez and Mercedes G. López",downloadPdfUrl:"/chapter/pdf-download/69917",previewPdfUrl:"/chapter/pdf-preview/69917",authors:[null],corrections:null},{id:"67785",title:"Metabolomic Discovery of Microbiota Dysfunction as the Cause of Pathology",doi:"10.5772/intechopen.87176",slug:"metabolomic-discovery-of-microbiota-dysfunction-as-the-cause-of-pathology",totalDownloads:955,totalCrossrefCites:6,totalDimensionsCites:6,hasAltmetrics:0,abstract:"In the twenty-first century, metabolomics allowed evaluating the profile of metabolites of various classes of compounds in the human body. The most important achievement of the metabolic approach is to obtain evidence of the intersection of human biochemical pathways and its microbiota. The effect of certain microbial metabolites on the work of key enzymes involved in the biotransformation of amino acids and other substances becomes more important in patients at risk of developing neurological and mental disorders and also contributes to the development of life-threatening conditions up to multiple organ failure after operations, injuries, and serious diseases. The authors of this chapter call the microbiota an “invisible organ,” emphasizing its functional significance, and not just taxonomy, as previously thought. This chapter will discuss the mutually beneficial integration of the metabolome/microbiome in the body of healthy people and will focus on the effects of microbiota dysfunction.",signatures:"Natalia V. Beloborodova, Andrey V. Grechko and Andrey Yu Olenin",downloadPdfUrl:"/chapter/pdf-download/67785",previewPdfUrl:"/chapter/pdf-preview/67785",authors:[null],corrections:null},{id:"68338",title:"Serum Metabolomics as a Powerful Tool in Distinguishing Trauma from Other Critical Illness Conditions",doi:"10.5772/intechopen.87145",slug:"serum-metabolomics-as-a-powerful-tool-in-distinguishing-trauma-from-other-critical-illness-condition",totalDownloads:626,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Critical illness is highly variable, complicating patient care and recovery. We have previously used metabolomics to investigate several causes of intensive care unit admission, seeking to assess changes in metabolism occurring with each condition. We present a meta-analysis of these serum metabolomes, exploring how the metabolomes differ with each condition. We also present how mass spectrometry-based metabolomics could be used for predictive monitoring. Serum metabolites were previously quantified using nuclear magnetic resonance spectroscopy in patients with traumatic injury, respiratory failure, pancreatitis, and combat trauma. Healthy controls are also included. Spectral features were analyzed with principal component analysis (PCA) to explore patterns in patients’ underlying conditions. PCA suggests trauma metabolic profiles, particularly combat casualties, differ from other conditions. Principal components 2 and 3, accounting for 16% of the variation in the model, distinguish samples obtained from trauma patients. Metabolomics is a powerful tool for quantifying variability in critical illness, highlighting trauma as separate from other conditions. This observation is in line with the -omics literature, which has described a massive global “genomic storm” in response to severe injury. Mass spectrometry highlights this extreme variability, which occurs in ICU patients but not healthy controls. With new technology, metabolomics could be used to bring faster, individualized patient care to the ICU.",signatures:"Elizabeth R. Lusczek",downloadPdfUrl:"/chapter/pdf-download/68338",previewPdfUrl:"/chapter/pdf-preview/68338",authors:[null],corrections:null},{id:"68857",title:"Chinese Medicines for Cancer Treatment from the Metabolomics Perspective",doi:"10.5772/intechopen.88924",slug:"chinese-medicines-for-cancer-treatment-from-the-metabolomics-perspective",totalDownloads:725,totalCrossrefCites:1,totalDimensionsCites:2,hasAltmetrics:1,abstract:"Cancer is one of the most prevalent diseases all over the world with poor prognosis and the development of novel therapeutic strategies is still urgently needed. The large amount of successful experiences in fighting against cancer-like diseases with Chinese medicine has suggested it as a great source of alternative treatments to human cancers. Cancer cells have been shown to own a predominantly unique metabolic phenotype to facilitate their rapid proliferation. Metabolic reprogramming is a remarkable hallmark of cancer and therapies targeting cancer metabolism can be highly specific and effective. Based on the sophisticated study of small molecule metabolites, metabolomics can provide us valuable information on dynamically metabolic responses of living systems to certain environmental condition. In this chapter, we systematically reviewed recent studies on metabolism-targeting anticancer therapies based on metabolomics in terms of glucose, lipid, amino acid, and nucleotide metabolisms and other altered metabolisms, with special emphasis on the potential of metabolic treatment with pure compounds, herb extracts, and formulations from Chinese medicines. The trends of future development of metabolism-targeting anticancer therapies were also discussed. Overall, the elucidation of the underlying molecular mechanism of metabolism-targeting pharmacologic therapies will provide us a new insight to develop novel therapeutics for cancer treatment.",signatures:"Wei Guo, Hor-Yue Tan, Ning Wang and Yibin Feng",downloadPdfUrl:"/chapter/pdf-download/68857",previewPdfUrl:"/chapter/pdf-preview/68857",authors:[{id:"14428",title:"Prof.",name:"Yibin",surname:"Feng",slug:"yibin-feng",fullName:"Yibin Feng"},{id:"175059",title:"Dr.",name:"Ning",surname:"Wang",slug:"ning-wang",fullName:"Ning Wang"},{id:"201389",title:"Mrs.",name:"Wei",surname:"Guo",slug:"wei-guo",fullName:"Wei Guo"},{id:"281069",title:"Dr.",name:"Hor Yue",surname:"Tan",slug:"hor-yue-tan",fullName:"Hor Yue Tan"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:{id:"17",series:{id:"11",title:"Biochemistry",issn:"2632-0983",editor:{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"5",totalChapterViews:"0",totalEditedBooks:"6",institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}}}},tags:null},relatedBooks:[{type:"book",id:"10442",title:"Cyanobacteria",subtitle:"Recent Advances in Taxonomy and Applications",isOpenForSubmission:!1,hash:"2fec78743d3f973c80881957ce3e6d79",slug:"cyanobacteria-recent-advances-in-taxonomy-and-applications",bookSignature:"Wael N. Hozzein",coverURL:"https://cdn.intechopen.com/books/images_new/10442.jpg",editedByType:"Edited by",editors:[{id:"189233",title:"Prof.",name:"Wael N.",surname:"Hozzein",slug:"wael-n.-hozzein",fullName:"Wael N. 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The Sense of Places, Models and Applications",slug:"landscape-architecture-the-sense-of-places-models-and-applications",publishedDate:"September 19th 2018",bookSignature:"Amjad Almusaed",coverURL:"https://cdn.intechopen.com/books/images_new/6066.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"110471",title:"Prof.",name:"Amjad",middleName:"Zaki",surname:"Almusaed",slug:"amjad-almusaed",fullName:"Amjad Almusaed"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"221245",title:"Dr.",name:"María Jesús",middleName:null,surname:"Montero-Parejo",fullName:"María Jesús Montero-Parejo",slug:"maria-jesus-montero-parejo",email:"cmontero@unex.es",position:null,institution:null},{id:"223556",title:"Dr.",name:"Jin Su",middleName:null,surname:"Jeong",fullName:"Jin Su Jeong",slug:"jin-su-jeong",email:"jsbliss@gmail.com",position:null,institution:null},{id:"223557",title:"Prof.",name:"Julio",middleName:null,surname:"Hernández-Blanco",fullName:"Julio Hernández-Blanco",slug:"julio-hernandez-blanco",email:"juliohb@unex.es",position:null,institution:null},{id:"223558",title:"Prof.",name:"Lorenzo",middleName:null,surname:"García-Moruno",fullName:"Lorenzo García-Moruno",slug:"lorenzo-garcia-moruno",email:"lgmoruno@unex.es",position:null,institution:null}]},book:{id:"6066",title:"Landscape Architecture",subtitle:"The Sense of Places, Models and Applications",fullTitle:"Landscape Architecture - 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\r\n\tThe objective of this book is to make the food professionals acquainted with recent directions of the research work in food science. The different sections of this book project will describe the utilization of digital transformation in the food industry using the available applications of digital tools such as the internet of things (IoT), artificial intelligence (AI), sensor technologies, and blockchain. The effect of climate changes on the agro-industry will be discussed through the issues of climate changes, climate adaptation, agro-ecosystems, and environmental aspects and impacts. Recently, the food industry is subjected to unexpected new risks such as pandemics, lack of specific food supply, financial situations, and information technology problems so this too should be taken into consideration in the food science research work. As the food industry is a consumer-driven industry the continual improvement is a cornerstone in this industry. Recent technologies such as nanotechnology, membrane technology, and high-pressure technology besides the advanced analytical methods such as applications of the electron microscope and PCR would be covered.
",isbn:"978-1-80356-066-3",printIsbn:"978-1-80356-065-6",pdfIsbn:"978-1-80356-067-0",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,isSalesforceBook:!1,hash:"086633aee9a7b3ec134fb3a465418eac",bookSignature:"Prof. Yehia El-Samragy",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/11741.jpg",keywords:"Internet of Things, Artificial Intelligence, Blockchain, Climate Change, Agroecosystems, Pandemics, Information Technology Problems, Lack of Specific Food Supply, Nanotechnology, High-Pressure Technology, PCR, Membrane Technology",numberOfDownloads:18,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 2nd 2021",dateEndSecondStepPublish:"December 23rd 2021",dateEndThirdStepPublish:"February 28th 2022",dateEndFourthStepPublish:"May 19th 2022",dateEndFifthStepPublish:"July 18th 2022",remainingDaysToSecondStep:"5 months",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:"Professor Emeritus of Food Science, International Expert Trainer of Food Safety and Quality Management Systems, IRCA Lead Auditor/Tutor of QMS, and Food Safety, FSPCA Lead Instructor of PCQI and FSVP courses, registered Tutor of Highfield Food Safety and HACCP",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"81644",title:"Prof.",name:"Yehia",middleName:null,surname:"El-Samragy",slug:"yehia-el-samragy",fullName:"Yehia El-Samragy",profilePictureURL:"https://mts.intechopen.com/storage/users/81644/images/system/81644.jpg",biography:"Dr. El-Samragy has over four decades of a professional career bridged between academia and industry. He is Professor Emeritus of Food Science at Ain Sham University, Cairo, Egypt, and Visiting Research Professor at Cornell University, Ithaca, NY and Utah State University, Logan, UT, USA. He is an International Expert Trainer of Food Safety and Quality Management Systems. He worked as an Expert at some international organizations including FAO, UNIDO, UNDP, JECFA, ISO, USAID, ACDI-VOCA and DANIDA, in different projects of technology transfer, food standards, food product development, waste utilization, cleaner production, implementation of integrated management systems. He is IRCA Lead Auditor/Tutor of QMS, and Food Safety (HACCP & ISO/FSSC 22000) (IRCA Certificate # 01182132), and Lead Instructor, FSPCA Preventive Controls for Human Food Course (FSPCA Certificate # d16e213f) and FSPCA Foreign Supplier Verification Programs (FSPCA Certificate # d26bcf6b). 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From chapter submission and review to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"1014",title:"Food Additive",subtitle:null,isOpenForSubmission:!1,hash:"d5d05e31d794c4697626a5616a9fe077",slug:"food-additive",bookSignature:"Yehia El-Samragy",coverURL:"https://cdn.intechopen.com/books/images_new/1014.jpg",editedByType:"Edited by",editors:[{id:"81644",title:"Prof.",name:"Yehia",surname:"El-Samragy",slug:"yehia-el-samragy",fullName:"Yehia El-Samragy"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6548",title:"Food Safety",subtitle:"Some Global Trends",isOpenForSubmission:!1,hash:"de67614bdc5a5e48a1cf96f9e34e68a1",slug:"food-safety-some-global-trends",bookSignature:"Yehia El-Samragy",coverURL:"https://cdn.intechopen.com/books/images_new/6548.jpg",editedByType:"Edited by",editors:[{id:"81644",title:"Prof.",name:"Yehia",surname:"El-Samragy",slug:"yehia-el-samragy",fullName:"Yehia El-Samragy"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6418",title:"Hyperspectral Imaging in Agriculture, Food and Environment",subtitle:null,isOpenForSubmission:!1,hash:"9005c36534a5dc065577a011aea13d4d",slug:"hyperspectral-imaging-in-agriculture-food-and-environment",bookSignature:"Alejandro Isabel Luna Maldonado, Humberto Rodríguez Fuentes and Juan Antonio Vidales Contreras",coverURL:"https://cdn.intechopen.com/books/images_new/6418.jpg",editedByType:"Edited by",editors:[{id:"105774",title:"Prof.",name:"Alejandro Isabel",surname:"Luna Maldonado",slug:"alejandro-isabel-luna-maldonado",fullName:"Alejandro Isabel Luna Maldonado"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10359",title:"Landraces",subtitle:"Traditional Variety and Natural Breed",isOpenForSubmission:!1,hash:"0600836fb2c422f7b624363d1e854f68",slug:"landraces-traditional-variety-and-natural-breed",bookSignature:"Amr Elkelish",coverURL:"https://cdn.intechopen.com/books/images_new/10359.jpg",editedByType:"Edited by",editors:[{id:"231337",title:"Dr.",name:"Amr",surname:"Elkelish",slug:"amr-elkelish",fullName:"Amr Elkelish"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophile",surname:"Theophanides",slug:"theophile-theophanides",fullName:"Theophile Theophanides"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"80024",title:"Perturbation of Cellular Redox Status: Role of Nrf2, a Master Regulator of Cellular Redox",doi:"10.5772/intechopen.102319",slug:"perturbation-of-cellular-redox-status-role-of-nrf2-a-master-regulator-of-cellular-redox",body:'An equilibrium between the oxidants, reactive oxygen species and antioxidants attained by cell is defined as redox status of the cell, In case of any kinds of diseases or pathological conditions which disrupt this equilibrium thus creating an oxidized state, termed as oxidative stress [1]. This redox system essentially works in maintaining cellular homeostasis and cell survival. Reactive oxygen species (ROS) consist of reactive species like superoxide (O2−) and hydroxyl radical (HO), along with nonradical species such as hydrogen peroxide (H2O2). Reactive nitrogen species (RNS) contains nitrogen containing reactive species including nitric oxide (NO) and peroxynitrite (ONOO−). Agents that contribute to formation of these ROS/RNS may be exogenous sources like Chemicals (e.g., PCB), irradiation (i.e., UV irradiation, x-ray, gamma-ray) or atmospheric pollutants or they may be endogenous the mitochondria, where O2− is generated by electron leakage from complex I and III of the electron-transport chain, membrane-associated NAD(P)H oxidase, cytochrome c oxidase, and xanthine oxidase. In case of any oxidative stress experienced by the cell various enzymatic and non- enzymatic antioxidant systems present in the cell are ready to combat. A major class of enzymatic antioxidant systems include multiple isoforms of SOD, (SOD1, SOD2, SOD3) found in the extracellular matrix, cytoplasm, mitochondrial intermembrane space, nucleus, and lysosomes. Another enzymatic system which is responsible for conversion of reduced glutathione (GSH) to oxidized glutathione (GSSG), catalyzed by glutathione peroxidase (GPX) [2]. Non enzymatic systems include chemical antioxidants like glutathione (GSH), α-tocopherol (vitamin E), and ascorbic acid (vitamin C). GSH act as a cosubstrate in the reduction of H2O2 by GPx. It might also react with oxygen-free radical directly, similarly, vitamins E and C also reduce oxygen-free radicals. They act by trapping hydroxyl radicals and other reactive radicals and thus break radical chain reactions and form new less reactive radicals [3]. Reactive oxygen species (ROS) are reported to be involved in different cellular processes ranging from apoptosis and necrosis to cell proliferation and carcinogenesis. Reports confirm the ECS (endocannabinoid system), may play an important role in the regulation of cellular redox homeostasis [4]. Endocannabinoids such as AEA are also known to mediate some of their cellular responses by targeting the non-selective cation channel TRPV1, whose activation has been linked to increased ROS production, AEA has also been reported to target the PPAR family of nuclear receptors, whose activation is known to induce the expression of antioxidant enzymes, including catalase and glutathione peroxidase 3 [5]. Thioredoxins (Trx), function as hydrogen donors to thioredoxin-dependent peroxide reductases. These have a Cys-Gly-Pro-Cys active site, which is indispensable for redox regulatory functions of thioredoxins. Two isoforms of Trx have been observed, these are Trx1 (expressed in the cytoplasm and the nucleus) and Trx2 (expressed in the mitochondria), which are very crucial for cell survival. This implicates its protective role against reactive oxygen species [6].
Cellular Redox Homeostasis is determined by the ability of a cell to maintain the balance between the magnitude of generated oxidative stress and the rate of its detoxification [7] Maintaining the redox balance is important for proper function and responses of cells. Any disturbance in the redox homeostasis induces oxidative stress mediated signaling cascade that could lead to cell death or induce adaptive survival responses. Outcome of perturbation in the redox balance depends on the magnitude of oxidative stress induced inside the cell [8]. The intracellular “redox homeostasis” or “redox buffering” capacity is maintained primarily by glutathione (GSH oxidized / reduced) and thioredoxin (TRX oxidized/reduced) redox couples. GSH/GSSG ratio represents the major cellular redox buffer and it is therefore used as an indicator of the redox environment of the cell. GSH, Trx and glutaredoxin rectifies the thiol modifications due to oxidative stress. GSH reductase and Trx reductase reduces the GSSG and oxidized Trx at the expense of NADPH. The reducing nature of GSH and Trx is pivotal for the clearance of peroxides by peroxidase and peroxiredoxin [9]. Basal levels of reactive oxygen species (ROS) are endogenously produced in the mitochondria due to partial reduction of oxygen, inflammatory reactions and enzyme linked reactions viz. NAPH oxidase, Xanthine oxidase, cytochrome c oxidase [10]. Induction of mild oxidative stress activates redox sensitive pro-survival pathways like Nrf2 that protects against the oxidative damage. High oxidative stress leads to induction of apoptosis. Owing to their high reactivity, high levels of generated ROS react with the molecule including proteins, carbohydrates, lipids and DNA in the vicinity non-specifically (Figure 1).
Cellular redox homeostasis: Electron transport chain in mitochondria, endoplasmic reticulum and oxidases enzymes like NADPH oxidases and xanthine oxidase induces the generation of superoxide and peroxide radicals. The increase in hydrogen peroxide elevates the redox balance towards oxidative stress. Spatial-temporal regulation of the generated oxidative stress determines the cellular fate in term of apoptosis or cytoprotection. Activation & expression of transcription factors leading to the replenishment of antioxidant and cytoprotective machinery of the cell leads to restoration of redox balance.
This further results in impaired functioning of key cellular components directing the cell towards apoptosis [11]. However, generation of low levels of ROS acts as secondary messenger and activates numerous redox-sensitive pro-survival signaling pathways [12]. Spatio-temporal generation and regulation of ROS underlines their potential to contribute as secondary messenger from cell surface to the nucleus [13]. Scavenging of endogenous ROS can impair normal cellular response like production of cytokines and growth factors by T cells. Redox state of many proteins plays an important role during immune responses [14]. Critical cysteine residues present on proteins act as redox sensors and are prone to oxidation into sulfenic acids or disulphide formation or glutathionylation resulting in the modulation host immune responses [15]. The effect of oxidative stress on functions of these proteins depends on the concentration, duration and location of ROS generated inside the cell. A number of transcription factors and families have been identified which work in events of redox homeostasis or signaling, namely AhR, AP1, β-catenin, Egr-1, FOXO, HIF-1α, p53, NF-κB, Nrf2, Sp1, TTF. The present chapter is aimed at narrating the role of Nrf2 and NF-κB in redox environment and their redox regulation. Nrf2 being the master regulator is further detailed as putative target with therapeutic potential under multiple clinical settings.
NF-κB plays an important role in regulating the immune and inflammatory response. NF-κB is a ubiquitous transcription factor [16]. p52/p100, NF-κB p50/p105, C-REL, RELA/p65 and RelB constitute the Nuclear factor-κB (NF-κB) family of transcription factors. These factors mediate the transcription of target genes by binding to a specific DNA element, κB enhancer, as various hetero- or homo-dimers [17]. They also regulate the various biological responses such as immune responses, cell differentiation, cell proliferation, survival, stress response and inflammation. But the most studied and well-known function of NF-κB is in the inflammation, regulating the pro inflammatory cytokines, activation, differentiation and effector functions of T cells [18]. NF-κB has the ability to detect the stimuli such as infectious agents, UV radiation, ROS, Tissue injury, lipopolysaccharide (LPS), and free radicals which activate NF-κB [19]. The basic mechanism involves the tissue injury which activates NF-κB, dissociates IκB as a result of which the NF-κB enters the cell nucleus and activate the DNA to enhance the inflammatory cytokines [20]. Regulation of NF-κB activity is achieved through various post-translational modifications of the core components of the NF-κB signaling pathways. There are two pathways by which NF-κB is regulated; the canonical and the alternative pathway [21]. The canonical pathway is responsible for the installation of pro inflammatory cytokines, chemokines and other inflammatory mediators which directly engage into inflammation and act indirectly. Activation of the non-canonical NF-κB pathway involves different signaling molecules and leads to the predominant activation of the p52/RelB dimer. An “alternative” NF-κB pathway is activated by TNF-family cytokines—lymphotoxin b (TNFSF3) CD40 ligand (CD40L and TNFSF5), B cell activating factor (BAFF and TNFSF13B), and receptor activator of NF-κB ligand (RANKL and TNFSF11).
The canonical pathway is provoked by the pro-inflammatory cytokines, ligands of varied immune receptors and involves the rapid and transient activation of IκB kinase [22]. NF-κB activity at sites of inflammation is associated with activation of the canonical pathway and RelA- or cRel-containing complexes [23]. In the pathway, NF-κB/Rel proteins are tethered which are inhibited by IκB proteins. Pro inflammatory cytokines, lipopolysaccrahaide, growth factors and antigen receptors activate the IKK complex (IKKβ, IKKα and NEMO) [24]. The complex then phosphorylates IκB proteins which lead to ubiquitination and proteasomal degradation, freeing NF-κB/Rel complex. Active NF-κB/Rel complex is further activated by post transcriptional modifications and translocate to the nucleus, where either alone or in combination with other transcription factors including AP-1, Ets and STAT and induce target gene expression [25].
NF-κB2 p100/RelB complexes are inactive in cytoplasm. Signaling in LTβR, CD40, BR3 activate kinase NIK [26] which in turn activate IKKα complex that phosphorylate C terminal residue in NF-κB2 p100 which leads to ubiquitination and proteasomal processing to NF-κB2 p52 and translocate to nucleus to target gene expression [27]. The pathway regulates important aspects of immune functions, including lymphoid organ development, the cross-priming function of dendritic cells, B cell survival and germination center reactions, generation and maintenance of effector and memory t cells, antiviral innate immunity [28]. The pathway is responsible for inflammatory disease, kidney inflammation, metabolic inflammation and central nervous system inflammation [29]. Recent evidence suggests that NF-κB also has a role in regulating the activation of inflammasomes. Dysregulated NF-κB activation is a hallmark of chronic inflammatory diseases. Therefore, a better understanding of the mechanism that underlies NF-κB activation and pro-inflammatory function is of great significance for therapeutic strategies in the treatment of inflammatory diseases.
Imbalance in redox state is redox modulation. The redox state of cells controls the activation and inhibition of NF-κB, as in the state of oxidative stress that can both activate and inhibit NF-κB by targeting the upstream kinases [30]. Activation of NF-κB by regular signaling is well known, however NF-κB activation also depends on redox state of cells in three possible ways: (i) many NF-κB -activating substances cause the production of reactive oxygen species (ROS) superoxide, H2O2, lipoxygenase products or act as oxidants on their own, (ii) NF-κB activation can be caused by superoxide H2O2 or organic hydroperoxide in some cell lines when no physiological stimulation is present, and (iii) A wide range of NF-κB inhibitors inhibit NF-κB – activation and antioxidants that are chemically unrelated. These observations have led to a consensus that NF-κB activation is related to some oxidative reaction. Molecules like thioredoxin, escalates the activity of NF-κB to bind DNA under oxidative stress [31]. A component of dynein motor complex LC-8 also participates in redox regulation of NF-κB. It activates NF-κB on exposure of TNFα and results in ROS production which oxidizes LC-8 and its dissociation from IκBα thus leading to NF-κB activation. Reportedly, NF-κB activation has anti- oxidant and pro-oxidant roles, the former involves the suppression of ROS accumulation, autophagy promotion, Inhibition of JNK activation and increased anti-oxidant targets whereas the pro-oxidant role includes the induction of pro-oxidation genes. One of the most important molecules in regulating redox modulation is hydrogen peroxide, it has been a question of debate, if H2O2 is involved in redox activation of NF-κB. As indicated in literature, TNFα induced activation of NF-κB mediated by H2O2. TNFα is a strong activator of NF-κB, that induces superoxide formation in mitochondria. As in Wurzberg cells where H2O2 directly activates NF-κB. The findings were found to be inefficient when lymphoblastoid cell lines, Jurkat cells showed no results of NF-κB activation by H2O2 [31, 32]. Various exogenous and endogenous sources can enhance the redox reaction. Redox reactions play a huge role in inflammation specifically in lung inflammation where oxidative injury is most common due to its structure and function. ROS production is an immune response against inhaled pathogens and pollutants like cigarette smoke, automobile exhaust. Excess production of endogenous ROS leads to chronic inflammatory lung disease such as chronic obstructive pulmonary disease, asthama and pulmonary fibrosis. Oxidative stress produced by cigarette smoke activates NF-κB by activating IKK complex which interferes with the chromatin modifications that escalate the transcription of pro-inflammatory genes [33].
The nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) is a member of the cap ‘n’ collar (CNC) subfamily of basic region leucine zipper (bZip) transcription factors including nuclear factor erythroid-derived 2 (NFE2) and NRF1, NRF2, and NRF3. There are seven conserved NRF2-ECH homology (Neh) domains within NRF2 gene, with different functions to control NRF2 transcriptional activity. The bZip in the Neh1 domain acts to activate gene transcription by forming dimer with small musculoaponeurotic fibrosarcoma proteins (sMAF). Neh2 domain mediates NRF2 ubiquitination and degradation as it contains ETGE and DLG motifs which act together with Kelch domain of Kelch-like-ECH-associated protein 1 (KEAP1) [34]. The Neh3-5 domains find their role as transcriptional activation domains, Neh6 domain works to mediates Nrf2 degradation in cells experiencing oxidative stress. Neh7 domain mediates interaction with retinoic X receptor alpha (RXRα), which represses Nrf2 activity. It is involved in the control of development of labial and mandibular segment of Drosophila by basic leucine zipper DNA binding domain (bZip) homeotic gene [35].
Removal of Nrf2 alters the defense machinery of the cell against oxidative stress. Knocking out Nrf2 has no effect on the mortality of the mice. Basal level expression of Nrf2 in the cytoplasm ensures the production of cytoprotective proteins to exert normal physiological redox homeostasis [36]. Modulation in redox status is known to activate prosurvival redox sensitive Nrf2 pathway. Under normal condition Nrf2 is sequestered in cytoplasm by the inhibitor KEAP-1. Abrogation of KEAP-1 binding leads to translocation of Nrf2 to the nucleus mediated by nuclear localization signal. In nucleus Nrf2 forms a heterodimer with the co-transcription factor MAF. The heterodimers bind to the corresponding antioxidant response element and induces the expression of downstream cytoprotective and antioxidant enzymes [37]. The Nrf2 system is considered to be a major cellular defense mechanism against cellular oxidative stress. Nrf2 plays an important role in cellular defense and in improving the removal of ROS by activating downstream genes that encode phase II detoxifying enzymes and antioxidant enzymes, such as GCLM, NQO1, HMOX1, GPX, and glutathione S-transferases (GST) [38]. Nrf2 controls the expression of key components of the glutathione (GSH) and thioredoxin (TXN) antioxidant system, as well as enzymes involved in NADPH regeneration, ROS and xenobiotic detoxification, heme metabolism, thus playing a fundamental role in maintaining the redox homeostasis of the cell. Excessive ROS production causes oxidative stress to increase mitochondrial DNA damage, further promotes the activation of oncogenes or the inactivation of anti-oncogenes, which facilitates its tumorigenic signaling pathways and tumor progression. Nrf2/ARE pathway protects cells against oxidative stress via regulating the expression of Sestrin 2 gene as evident by monitoring the expression of downstream antioxidants. Sestrin 2 has strong antioxidant capacity and can provide cell with cytoprotective against various harmful stimuli. Sestrin blocks mTOR expression and mitigates the accumulation of ROS [39].
Redox regulation underlines the cellular homeostasis. Regulation of redox sensitive transcription factors play a pivotal role in determining the cellular fate. Nrf2 being a master regulator is at the focal point of maintaining and regulating the cellular redox equilibrium. Perturbation in redox equilibrium is known to modulate the Nrf2 activation and hence effect the cellular fate [19]. Spatio-temporal generation of oxidative stress determines the graded activation of redox sensitive mediators. Mild oxidative stress is known to activate Nrf2 pathway and increases the cytoprotective proteins. Redox based activation of Nrf2 is attributed to the presence of more than 20 critical cysteine residues present in the KEAP-1 protein (Figure 2) [40]. 273 and cys288 have been shown as critical for abrogating KEAP-1 mediated inhibition of Nrf2. Mutation in these residues render activation of Nrf2 by inhibiting the Cul3-E3-KEAP-1 mediated degradation of Nrf2. The mutation did not had any effect on the detachment of the KEAP-1:Nrf2 complex, thus allowing the nuclear translocation of free Nrf2. Further, cys151 was also implicated in redox modulator-based activation of Nrf2 pathway. Perturbation in cellular redox status by prooxidants have been shown to induce cellular oxidative stress and increase the glutathionylation of proteins. 1,4 Naphthoquinone treatment induced glutathionylation of KEAP-1 for inducing Nrf2 pathway owing to its prooxidant nature. Apart from the cytoprotective nature of Nrf2, its role as a redox sensitive anti-inflammatory transcription factor has been well documented. Multiple reports have highlighted redox modulation based modulating role of Nrf2 in ameliorating immune-pathologies [41]. Nrf2 knockout mice exhibited increased bronchial inflammation, prolonged inflammation, high susceptibility for autoimmune syndrome, elevated lymphocyte proliferation and impaired redox homeostasis. Nrf2 dependent proteins including HO-1 inhibits the cytokine secretion, leukocyte migration, adhesion and suppressed LPS induced production of tumor necrosis factor-a (TNF-a) and nitric oxide (NO) in murine macrophages. Ablation in HO-1 protein increases the susceptibility towards autoimmune diseases [42].
Redox regulation of Nrf2 pathway. Under non-stressed condition, Nrf2 is sequestered by its inhibitor KEAP-1 in the cytoplasm by inducing ubiquitin mediated Nrf2 degradation. Increase in ROS and electrophiles induces oxidative stress which results in oxidation of critical cysteine residues in the redox sensitive transcription factors. Cysteine residues of KEAP-1 are oxidized to release Nrf2 which translocates to the nucleus to express the downstream genes of antioxidant and cytoprotective potential. Thus, redox perturbation and tickling induces the Nrf2 pathway that act as master regulator for maintaining cellular redox equilibrium in turn governing the cellular fate.
Excessive reactive oxygen species are threat to cells redox homeostasis which are major cause of oxidative stress leading to maladies like cellular dysfunction in aging, cardiovascular disease, renal dysfunction, diabetes, cancer is some to name a few. Antioxidant therapies play an important role in combating the progress of these diseases but the results are not satisfactory therefore there is an urgent need for a solution which activates endogenous antioxidant defenses. The redox-sensitive transcription factor NF-E2 related factor 2 (Nrf2) plays a significant role in synchronizing cellular antioxidant defenses and maintaining redox homeostasis [43]. Nrf2 is the “master regulator” of the antioxidant response, it modulates the expression of many genes, that include antioxidant enzymes, immune and inflammatory responses, tissue remodeling and fibrosis, carcinogenesis and metastasis. NRF2 activation by Keap1 binding is one of the major pathways that senses the oxidative stress, particularly there are Four reactive cysteine residues identified in Keap1 are most likely nominees for being the direct sensors of oxidative stress, various alternative mechanisms for Nrf2 activation were discovered, which are dependent upon kinase pathways, these include mitogen-activated protein kinases (MAPK), phosphatidylinositol-3 kinase and atypical protein kinase(s) C. Cell culture experiments report many compounds which show the ability to activate Nrf2. Large number of Nrf2 activators are principally naturally-occurring and plant-derived such as sulforaphane and curcumin and found in foods, but synthetic compounds have also shown to act as activators for instance bardoxolone methyl [44].
The Therapeutic potential of Nrf2 and its activators have been studied in various diseases. Some of them are as follows:
It is the leading cause of chronic kidney disease, some mechanisms contribute to the onset and pathogenesis of diabetic nephropathy, including genetic and hemodynamic factors, oxidative stress, and cytokine signaling. Diabetes triggers oxidative stress through different ways, such as advanced glycation end-product accumulation and activation of polyol pathway, protein kinase C pathway, and renin angiotensin-aldosterone system. Loss or decrease in expression of SOD or glutathione in renal diseases are overcome by restoring and check the progression of disease. Nrf2 regulates expression of genes through ARE (antioxidant response elements) in their promoters to neutralize free radicals and accelerate removal of environmental toxins. Protective role of Nrf2 against renal damage has been demonstrated on streptozotocin induced diabetic rats, wherein it was shown that it slows the progression of diabetic nephropathy, Nrf2-mediated protection works through the negative regulation of TGF-b1 and p21/WAF1Cip1 (p21) [45]. Reports suggest the Nrf2-dependent anti-oxidative and anti-inflammatory effects of digitoflavone in streptozotocin-induced diabetic nephropathy,
Systematic studies of carcinogenesis specify an important role of endogenous oxidative damage to DNA, and an imbalance of cellular redox homeostasis that is balanced by elaborate defense and repair processes [49]. Pancreatic cancer is the most fatal diseases, it has very high rate of metastasis, Keap1-Nrf2 pathway is an emerging target for PC prevention and therapy. Certain modulators like UHRF1 (ubiquitin-like containing PHD and RING finger domains 1) is overexpressed in pancreatic cancer and are correlated to tumor growth. UHRF1 suppresses Keap1 expression by promoter methylation, this leads to Nrf2 activation. MBD 1 and p62 have been reported to inhibit ROS and promote tumor growth and drug resistance by inducing Nrf2 accumulation, nuclear translocation and activation. Nrf2 activation by a has also been found to inhibit PC cell growth and induce apoptosis by upregulating HO-1 [50]. The compound D3T (3
Pulmonary fibrosis is a progressive and irreversible disease; it is characterized by an increase in differentiation and of fibroblasts to myofibroblasts and excessive accumulation of extracellular matrix in lung tissue. A study reports antifibrotic function of sulforaphane (SFN), an NRF2 activator, was largely dependent on a long noncoding RNA [54]. Therapeutic potential of thymoquinone (TQ) in bleomycin-induced lung fibrosis (BMILF) were also investigated and it was seen that it decreases expressions of Nrf2, Ho-1 and TGF-β. Nrf2/Ho-1 signaling pathway is a principal target for TQ protective effect against BMILF in rats [55]. The protective role of Nrf2 is mediated by PPARγ in hypoxia-induced Acute Lung Injury (ALI). Reports reveal that overexpression of Brg1 increases Nrf2 activity and reduces ROS and inflammatory factors in lung tissues. In lipopolysaccharide (LPS)-induced lung inflammation the defensive role of the PI3K/Akt-dependent activation of the Nrf2-HO-1 pathway was revealed in mice treated with desoxyrhapontigenin. Nrf2 knockout resulted in a worsening of asthma symptoms. Protective role of Nrf2 in emphysema induced mice can be correlated by its activation in alveolar macrophages. The role of Nrf2 dysfunction in COPD may be the result of loss of DJ-1. DJ-1 overexpression activates Nrf2 and inhibits apoptosis of alveolar type II cells that are undergoing Cigarette smoking-induced oxidative stress and inflammatory response. DJ-1 induces the activation of Nrf2 and increases the expression of downstream antioxidant machinery to reduce the oxidative stress. The underlines anti-inflammatory effects are attributed to the expression of HO-1. These findings highlight the role of DJ-1 as putative target for cigarette smoking induced lung diseases [56].
Neurodegenerative conditions may be results of various primary causes which include including expression of certain gene alleles, toxicant administration, aging, protein aggregation, proteasomal or autophagic dysfunction, inflammation, neuronal apoptosis, oxidative stress, mitochondrial dysfunction, and interactions between neurons and glia. The earliest degenerative condition to be associated with oxidative stress was aging. Some diseases characterized as neurodegenerative are Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and Alzheimer’s disease, Huntington’s disease, Friedrich’s ataxia, multiple sclerosis, and stroke. Nrf2 activation provides neuroprotection against oxidative stressors and mitochondrial toxins, including hydrogen peroxide, tert-butyl hydroperoxide, 6-hydroxydopamine, 3-nitropropionic acid (3-NP), 1-methyl-4-phenylpyridinium (MPP), and rotenone [57]. In various studies conducted water derivative of artemisinin namely artesunate and lipid soluble derivative artemisinin, artemether both show to enhance the activation of Nrf2 via increasing its nuclear translocation and binding to downstream antioxidant response elements, as well as through suppressing ROS-dependent p38 MARK and NF-κB pathways [58]. Report suggests that SFN, an isothiocyanate compound that occurs naturally and can be derived from cruciferous vegetables such as broccoli is capable of activating Nrf2, Results show that SFN is able to cross the blood brain barrier, activate Nrf2-dependent gene expression in the basal ganglia, eventually protecting nigral dopaminergic neurons from cell death induced by MPTP. Wide variety of bioactive compounds like resveratrol, curcumin, naphthazarin, genistein, and carnosic acid and berberin have been reported as Nrf2 activators that show positive effects in neurodegenerative disorders by protecting dorsal root ganglion (DRG) neurons from glucose-induced injury also by antioxidant activity in primary spinal cord astrocytes exposed to H2O2 [59].
Cellular redox equilibrium is pivotal for normal cellular functioning and responses. Impairment in regulation and maintenance of redox homeostasis underlines the pathogenesis of multiple associated diseases. Thus, identifying the key players in redox regulation is of prime interest. Nrf2 and NF-KB are the two most pivotal and embroiled redox sensitive transcription factors that underlines the maintenance of redox balance. Thus, the two pathways are at the epicenter of investigation with clinical significance. The Nrf2 is the master regulator of cellular redox status. The Nrf2 and its dependent genes are responsible for cytoprotection, immunoregulation, maintaining cellular antioxidant levels, reducing drug toxicities etc. Presence of multiple critical cysteine residues in KEAP-1, inhibitor of Nrf2, renders redox sensitivity in activation of Nrf2 pathway. Aberrant expression and regulation of Nrf2 pathway has been implicated in various pathologies including cancer, diabetes, neurodegeneration etc. Multiple researchers have demonstrated the targeting of Nrf2 as key strategy to curb inflammation and associated disorders. Apart from Nrf2, another redox sensitive transcription factor is NF-κB. Aberrant activation of NF-κB pathway has been implicated in inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κB also contains cysteine residues which act as sensors for redox modulation. Recent advances have highlighted the cross talk between Nrf2 and NF-κB as putative target for strategic drug development. Further, in depth clinically relevant exploration of the cross talk is warranted. The triangulate interplay of cellular redox, Nrf2 and NF-κB have immense potential to generate the therapeutic benefits via serving a putative target for discovering and developing novel drugs.
There is no actual or potential conflict of interest.
Hair is made of several proteins, the principal protein that compound the fibrous structure of the hair is keratin, in addition to keratin, which has a high content of the amino acid cysteine, the hair also contains water, lipids, minerals, and the pigment melanin.
\nThe hair shaft (the visible fiber that is growth above the skin), is a fiber with a variety of color depending of the melanin content that pigmented the keratin fiber. The dermal element in the hair follicle is the dermal papilla, which is majorly former by fibroblast cells, this dermal element controls the hair cycle.
\nThe fiber of the hair, the hair shaft, grows from the hair follicle which is a tubular structure that forms a bulb around the matrix of the hair bulb, specialized dermal stem cell and different types of keratinocytes, from this hair bulb that form the dermal papilla the hair shaft growth by division of proliferative cells, thus cells goes to a process of differentiated, keratinized, and pigmented in the hair follicle to form the hair shaft in a cycling manner. The diameter of the hair shaft is directly related to the size of the papilla, and allows us to define the miniaturized hairs and normal hair.
\nThe hair structure is composed by concentric layers that forms the hair follicle, the medulla which is the center is includes the cortex and outwards the cuticle of the cortex, and is surrounded by the inner and outer root sheath, and all the mini-organ is surrounded by connective tissue.
\nThe functional aspect of hair is not only to protect from radiation, heat or cold and any extern agent but also contribute to the appearance and personality. The loss of the hair contributes to psychological, social and psychosocial problems, generating a cosmetic and social impact in our society.
\nThe hair follicle has the unique capacity of undergoing periods of growth (anagen), regression (catagen), and rest (telogen and exogen) before regenerating itself to restart the cycle [1, 2, 3, 4] (Figure 1). This dynamic cycling capacity enables mammals to change their coats, and for hair length to be controlled on different body sites [5].
\nHair cycle stages scheme, phase of growth (anagen), regression (catagen), and rest (telogen) before regenerating itself to restart the cycle.
Unlike what is observed in many animals in which the pelage synchronously passes from one phase of the cycle to other all stages of growth cycle are simultaneously found in the human, the growth pattern is a mosaic where the hair cycling staging of one hair root is completely independent of it nearest hair follicle, meaning that each follicular unit (FU) can contain follicles in different stages at any given time. In healthy individuals, 80–90% of follicles are in the anagen phase, 1–2% in the catagen phase, and 10–15% in the telogen phase [6]. The hair grows around one centimeter a month, and has a variable growth speed being faster in the summer than in winter. The growth phase, or anagen phase, lasts an average of 3–5 years. This normal hair-growth cycle can be modified or by internal or external factors such as hormones, stress, sun, disease, exposure to environmental pollution, drugs and smoking. This changes in the growth cycle and quality of hair can leads to hair loss by a shortening of the anagen phase, a premature ingression of the catagen phase, the prolongation of the telogen phase or a loss of the hair follicle function [6, 7]. Common hair loss is medically named as alopecia, and can be suffer by men and women.
\nResearch has shown that in hair loss, the percentage of telogen follicles is increased, while the percentage of anagen and catagen follicles is reduced. A healthy individual loses approximately 100–150 hairs per day [6]. Cell-signaling pathways in hair follicular cells resulting in the induction of apoptosis, changes in usual pattern of hair cycling, inducing the hair follicle to turn into regression or resting phase and thinning or fracture of the hair shaft leads to progressive hair loss and alopecia [7].
\nHair loss is a universal problem for numerous people in the world, is a disorder in which the hair falls out from skin areas such as scalp, the body and face. Multiples factors contribute to hair loss including genetics, hormones, nutritional status, and environmental exposure (exposure to radiations, environmental toxicants…), medications and nutrition.
\nAndrogenic alopecia can be suffered by women and men and the androgens hormones are the most important of the factors that cause the hair lost patron characterized by a miniaturized of the hair follicles that leads to hair lost in the frontal to parietal area.
\nOther forms of hair loss are for example caused by immunogenic hair loss, like alopecia areata, this is characterized by a spot of hair lost all around the scalp. The approved therapies such as finasteride and minoxidil, are the traditional medication used for this hair lost diseases, a few others are in progress, like a wide variety of diverse phytochemicals, including those present in ginseng, the ginsenosides which have demonstrated hair growth-promoting effects in a large number of preclinical studies [7].
\nAndrogenic baldness (androgenic alopecia) and circular/spot baldness (alopecia areata) are the most common forms of hair loss. The first is characterized by high sensitivity of the hair follicles to DH, while the second is induced by an autoimmune reaction [8, 9]. Hair also possesses its own immune system, the failure of which can lead to spot baldness (alopecia areata).
\nAlopecia is extended all round the world, reaching nowadays approximately to 10 million patients suffering from alopecia. Considering the pathological background of alopecia and its impact on an individual’s health and social value, there is now a growing interest in the development of novel therapeutics for its medical management [7].
\nGiven the negative psychosocial impact of hair loss, patients follow different therapies, conventional treatments such as the two medications approved by the United States Food and Drug Administration (US-FDA): Minoxidil and Finasteride, for the treatment of alopecia.
\nFinasteride has a potent effect against androgens, being non-steroidal, it has shown to prevent male and female hair loss through the inhibition of type II 5α-reductase, which affects androgen metabolism avoiding the conversion of free testosterone into 5α-dihydrotestosterone, playing an important role in the pathogenesis of androgenetic alopecia in men and women [10].
\nThe effect of minoxidil as hair growth stimulating has been known over last decades, since it was introduced in the early 1970 as a treatment for hypertension. But yet the basic mechanism of action on the hair follicle is not clearly understood [11, 12].
\nThese drugs work improving the quality of the hair follicles and reducing the hair lost but exhibit certain adverse effects, such as allergic contact dermatitis, erythema, and itching, and also stop recommended guideline of minoxidil leads to recurrence of alopecia and a prolonged use of finasteride causes male sexual dysfunction and appears as a major cause of infertility and teratogenicity in females.
\nPatient that do not see significant hair restoration with conventional therapies or suffer side effects often change from these conventional treatments to alternative medicine trying new treatments from the vast resources of natural products, in an attempt to find safe, natural and efficacious therapies to restore the hair.
\nNatural products as it is known in the market “Dietary supplements” includes diverse subgroups like vitamins, probiotics, minerals, herbs, extracts, gels that do not require Food and Drug Administration (FDA) approval [13].
\nTo treat hair loss are available treatments using amino acids, caffeine, capsaicin, curcumin, garlic gel, onion gel and extract, cinnamon,
Ginseng is an ancient herbal remedy that was recorded in The Herbal Classic of the Divine Plowman, the oldest comprehensive Materia Medica, which was scripted approximately 2000 years ago [9].
\nAmong different species which are known as ginseng,
Nowadays has gained fame as one of the most popular herbs originating from Eastern Countries, because contemporary science has revealed that ginseng contains a wide variety of bioactive constituents, especially a group of saponin compounds collectively known as ginsenosides, which have been proposed to account for most of the diverse biological activities, including the hair-growth potential of ginseng [9]. Ginsenosides can be classified, depending on the number of hydroxyl groups available for glycosylation via dehydration reactions, as protopanaxadiol (PPD) and protopanaxatriol (PPT). Common PPD-type ginsenosides include ginsenosides Rb1, Rb2, Rc, Rd., Rg3, F2, Rh2, compound K (cK), and PPD, whereas PPT-type ginsenosides include Re, Rf, Rg1, Rg2, F1, Rh1, and PPT [9] and malony ginsenosides mRb1, mRb2 and mRbc [15]. Ginseng extract or its specific ginsenosides have been tested for their potential to promote hair growth.
\nThe major bioactive constituents of ginseng are ginsenosides and there has been evidences suggesting that promote hair growth by enhancing proliferation of dermal papilla and preventing hair loss via modulation of various cell-signaling pathways [9, 16, 17].
\nThe role of 5α-reductase enzyme in the hair-loss process has been well-documented [18], affects androgen metabolism, and it is the pathway how drugs approved are used nowadays.
\nNovel therapeutics ways for the management of hair loss and alopecia improving hair-follicle proliferation and reducing hair-loss need new targets (Figure 2). These targets include, matrix metalloproteinases (MMPs), extracellular signal-regulated protein kinase (ERK), and Janus-activated kinase (JAK), the activation of the proliferation by WNT/Dickkopf homolog 1 (DKK1), sonic hedgehog (Shh), vascular endothelial growth factor (VEGF), apoptosis inhibition by transforming growth factor-beta (TGF-β).
\nThe effect of the 5α-reductase enzyme, dihydrotestosterone, and the growth factor TGF-β on hair loss and the potential targets of ginseng in hair growth and loss.
Photo aging is skin damage induced by radiation exposure (Sun exposure) characterized by different inflammatory responses to ultraviolet radiation (UVR). Excessive UV irradiation is known to cause skin photo damage by release of oxidative species which leads to skin inflammation, and keratinocyte cell death producing photo aging and carcinogenesis.
\nThere are evidences that suggest that misbalances in the hair-growth cycle, affecting keratinocyte and dermal papilla growth [19] is cause by UVR exposure not only producing the damage of the hair shaft as an extracellular tissue, as it is clearly evident but also alters the molecular growth [19].
\nThe Reactive Oxidative Species (ROS) accumulation and activation of matrix metalloproteinase (MMPs), a tissue-degrading enzymes, produced by UV irradiation compromises dermal and epidermal structural integrity [9].
\nThe inhibitory effect of ginsenosides on UVB-induced activation of MMP2 suggests the potential of these ginseng saponins in hair-growth regulation [9]. Ginsenosides Rb2 [20] and 20 (S) PPD, have been reported to reduce the formation of ROS and MMP-2 secretion in cultured human keratinocytes (HaCaT) cells after exposure to UVB radiation. Ginsenoside Rg3 20 (S), reduced ROS generation in HaCaT cells and human dermal fibroblasts without affecting cell viability. The 20 (S) Rg3 also attenuated UVB-induced MMP-2 levels in HaCaT cells [21]. Ginsenoside Rh2 reduced UVB radiation-induced expression and activity of MMP-2 in HaCaT cells, but UVB-induced ROS formation was only suppressed by 20 (S)-Rh2 [22].
\nGinsenosides extracts from the Ginseng radix have shown attenuates radiation-induced cell death in the skin, improving hair growth. Ki67 positive number of cells and Bcl2 protein expression, an antiapoptotic protein, are induced by Total-root saponins and ginsenoside Rb1 diminishing apoptotic cells in UVB-exposed human keratinocytes [9, 23]. Ginsenoside F1, an enzymatically modified derivative of ginsenoside Rg1, by maintaining a constant level of the antiapoptotic protein Bcl-2 expression in UVB-irradiated HaCaT cells, protect keratinocytes from radiation-induced apoptosis [9, 24].
\nSkin aging is a multifactorial process consisting of two distinct and independent mechanisms: intrinsic and extrinsic aging.
\nGinsenosides, extracted from Ginseng have been tested in several studies in antiaging [25, 26]. This antiaging effects, of ginseng extract and ginsenosides is produced by maintaining skin structural integrity and regulating hair-growth by stimulating wound healing cells, collagen and hyaluronic acid.
\nLee et all incubates fibroblasts, which are key wound-healing cells, with
Wrinkle formation, is associated as marker of dermal aging and present a reduced level of hyaluronan in the dermis [29]. On HaCaT cell treated with major ginseng metabolite (compound K, 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol) were report that hyaluronan synthase2 (HAS2) gene is one of the most significantly induced genes [30] and also was tested that topical application of compound K on mouse skin and shows elevated the expression of hyaluronan synthase-2 [30]. The hyaluronan synthase-2 is an enzyme essential to hyaluronan synthesis, hyaluronan is a major component of most extracellular matrices that has a structural role in tissues architectures and regulates cell adhesion, migration and differentiation.
\nThese antiaging effects of ginseng extracts through Src kinase-dependent activation of ERK and AKT/PKB kinases in the dermis and papillary dermis result in improved skin health, thereby ensuring hair-follicle health and a regular hair cycle [9, 30].
\nThe exposure to androgens is the major triggers for hair loss is which in most cases is genetically predetermined in androgenic alopecia patients [9, 31, 32].
\nThe androgen that mainly plays a role in altering hair cycling is 5α-dihydrotestosterone (DHT), which is a metabolite of testosterone. The conversion of testosterone to DHT is mediated by the 5α-reductase (5αR) enzyme in each follicle [33, 34] (Figure 2). Treatment with 5α-reductase inhibitors, e.g., finasteride, prevents the development of alopecia and increases scalp-hair growth [9].
\nTopical application of ginseng extract or ginsenosides was reported to enhance hair growth. Rhizomes of
Major components of hair regenerative capacity such as linoleic acid (LA) and β-sitosterol (SITOS) were significantly restored with Red Ginseng Oil (RGO) after testosterone (TES)-induced delay of anagen entry in C57BL/6 mice, also RGO and its major components reduced the protein level of TGF-β and enhanced the expression of anti-apoptotic protein Bcl-2, suggesting that RGO is a potent novel therapeutic natural product for treatment of androgenic alopecia [37].
\nRed Ginseng Extract (RGE) and ginsenosides protect hair matrix keratinocyte proliferation against dihydrotestosterone (DHT)-induced suppression and affects the expression of androgen receptor.
\nMoreover, RGE, ginsenoside-Rb1, and ginsenoside-Rg3 at lower levels that have been shown to inhibit 5a-reductase [35] inhibit the DHT-induced suppression of hair matrix keratinocyte proliferation and the DHT-induced upregulation of the mRNA expression of androgen receptor in hDPCs [16].DHT is the product of testosterone and does not require the activity of 5a-reductase to affect hair follicles, and the inhibitory effect of DHT on hair growth is mediated by the androgen receptor in DPCs [38] These results suggest that red ginseng may promote hair growth in humans through the regulation of androgen receptor signaling [16].
\nMajeed et al. review the recent perspectives of ginseng phytochemicals as therapeutics in oncology and explain the chemotherapeutic effect of ginsenoside as result of its appetites, ant proliferative, anti-angiogenic, anti-inflammatory and anti-oxidant properties [39]. The anticancer effect of ginseng was proven in various types of cancer: breast, lung, liver, colon and skin cancer. It increases the mitochondrial accumulation of apoptosis protein and down regulate the expression of anti-apoptotic protein, reducing cancer development. It also aids in the reduction of alopecia, fatigue and nausea, the known side effects of chemotherapeutic drugs [39].
\nAlopecia induced by chemotherapy is one of the most distressing side effects for patients undergoing chemotherapy. One drug used as chemotherapy is Cyclophosphamide (CP), also known as cytophosphane\n. Cyclophosphamide metabolite, 4-hydroperoxycyclophosphamide (4-HC) inhibited human hair growth, induced premature catagen development, and inhibited proliferation and stimulated apoptosis of hair matrix keratinocytes inducing the side effect of alopecia. In human hair follicle organ culture model pre-treatment with Korean Red Ginseng (KRG) before cyclophosphamide metabolite Dong In Keum et all shows that KRG suppress 4-HC-induced inhibition of matrix keratinocyte proliferation and stimulation of matrix keratinocyte apoptosis, playing a protective effect on 4-HC-induced hair growth inhibition and premature catagen development. Moreover, KRG restored 4-HC-induced p53 and Bax/Bcl2 expression [17].
\nDifferent intracellular signaling pathways are involving and plays a critical role in stimulating hair growth by promoting dermal papillary-cell proliferation.
\nHair growth is promote by Ginsenoside Rg3 upregulating Vascular Endothelial Growth Factor (VEGF) expression [36].VEGF is a signaling protein which is released from the epithelium and increases the angiogenesis of the hair follicle [9, 40, 41, 42]. Was also demonstrate by Shin et al. that Rg3 increased the proliferation of human dermal papillary cells, associating this proliferation with an upregulation of mRNA expression of VEGF also stimulated stem cells by upregulating factor-activating CD34 and CD8 [36] and promoted hair growth even more than minoxidil in mouse [43] it was conclude that Rg3 might increase hair growth through stimulation of hair follicle stem cells [36].
\nRGE and ginsenoside-Rb1 enhanced the proliferation of hair matrix keratinocytes, human hair-follicle dermal papillary cells (hDPCs). Treated hair with RGE or ginsenoside-Rb1 exhibited substantial cell proliferation and the associated phosphorylation of ERK and AKT [16], it was recently demonstrated that ERK activation plays an important role in the proliferation of hDPCs [42] and AKT mediates critical signals for cell survival and also regulates the survival of DPCs as an antiapoptotic molecule [9, 16, 44] proliferation and the prolongation of the survival in the hDPCs by red ginseng may be mediated by the ERK and AKT signaling pathway [9, 16].
\nHuman DPC treatment with Gintonin-enriched fraction (GEF) stimulated vascular endothelial growth factor release. Topical application of GEF and minoxidil promoted hair growth in a dose-dependent manner. Histological analysis showed that GEF and minoxidil increased the number of hair follicles and hair weight [45].
\nThe Bcl-2 family proteins is notable for their regulation of apoptosis machinery, a form of programmed cell death, the member of this family either acts as antiapoptotic or pro apoptotic in nature. During the hair cycle, the dermal papillary cells (DPC) is the only region where Bcl-2 is expressed consistently and is considered to resist apoptosis [9, 46, 47, 48]. In mice Fructus
Shh/Gli and Wnt/β path way and related proteins (Shh (Sonic hedgehog,) Smoothened (Smo), β-catenin, Cyclin D1 Cyclin E and Gli1 (glioma-associated oncogene homolog)) are associated to hair regeneration, promoting telogen-to-anagen transition, hair follicle formation and growth. [50, 51, 52, 53, 54, 55, 56].
\nWingless-type integration-site (WNT) signaling plays a key role in hair-follicle development. Activation of WNT signaling is necessary for initiation of follicular develop, the blockade of WNT signaling by overexpression of the WNT inhibitor, Dickkopf Homolog 1 (DKK1), prevents hair-follicle formation in mice [50] and inhibited hair growth [9, 50].
\nβ-catenin signaling is essential for epithelial stem-cell fate since keratinocytes adopt an epidermal fate in the absence of β-catenin [51], and this signaling pathway is related to WNT [52] affecting hair follicle placodes formation, when β-catenin is mutated during embryogenesis, formation of placodes that generate hair follicles is blocked [53].
\nThe role of TGF-β in hair loss has been documented through the study revealing that treatment with a TGF-β antagonist can promote hair growth via preventing catagen progression [57]. Also through the activation of TGF-β and brain-derived neurotrophic factor (BDNF), it was describe that it was enhanced the transition from the anagen to the catagen phase [58].
\nSince TGF-β1 induces catagen in hair follicles and it is closely related to alopecia progression it can be say that acts as a pathogenic mediator of androgenic alopecia [57, 59] and red ginseng extract can delay the catagen phase and holds the potential to promote hair growth, thought downregulation or inhibition of the TGF-β pathway.
\nOn Young Go Kim investigation was concluded that on ultraviolet B (UVB)-irradiated skin aging in mice, oral administration of Red Ginseng extract protects from skin damage induced by ultraviolet B (UVB)-irradiation, increases of skin thickness and pigmentation, reduction of skin elasticity, inhibited the increases of epidermis and corium thickness. The administration of Red Ginseng extract exert the protective action on UVB-radiation skin aging inhibiting the increase of skin TGF-beta1 content induced by UVB irradiation [60].
\nFurthermore on Zheng Li the hair-growth-promoting effects of Protopanaxatiol type ginsenoside Re were associated with the downregulation of TGF-β-pathway-related genes, which are involved in the control of hair-growth phase-transition-related signaling pathways [61]. On their study shows that topical administration of ginsenoside Re on to the back skin of nude mice for up to 45 days significantly increased hair-shaft length and hair existent time, and stimulated hair-shaft elongation in the ex vivo cultures of hair follicles isolated from C57BL/6 mouse [61].
\nThe hyper activation of the c-Jun-N-terminal kinase (JNK) pathway in associate with an activation of TGF-β-induced hair loss. Korean red ginseng has been attributed to exert protective effects onTGF-β-induced hair loss by the inhibition of JNK on radiation-induced apoptosis of HaCaT cells [62].
\nBy promoting telogen-to-anagen transition of follicular cells and epidermal growth, Shh/Gli regulates hair-follicle development, growth and cycling [54, 55]. Shh−/− mice develop have abnormal hair follicular cells in the dermal papillae and blocking Shh activity mice diminished hair growth, this results indicates the importance of Shh signaling in hair-growth promotion [56].
\nAndrogenetic alopecia is related to testosterone (TES)-induced delay of anagen phase and hair loss. In C57BL/6 mice Red-ginseng oil (RGO) reversed testosterone-induced suppression of hair regeneration through early inducing anagen phase by up-regulating the expression of Shh/Gliand Wnt/β pathway-related proteins, Shh, Smoothened (Smo), β-catenin, Cyclin D1 Cyclin E and Gli1. Additionally, RGO reduced the protein level of TGF-β but enhanced the expression of anti-apoptotic protein Bcl-2 [37] suggesting that RGO is a potent therapeutic natural product for treatment of androgenic alopecia possibly through hair re-growth activity [37].
\nThe signaling pathway and anagen induction effect of ginsenoside F2 were investigated and compared with finasteride on the effect of hair growth induction in Heon-Sub Shin at all paper [43] where MTT assay results indicated cell proliferation in human DPC increased a 30% with ginsenoside F2 treatment compared to finasteride [43]. Studding the expression of β-catenin and its transcriptional coactivator Lef-1, the Ginsenoside F2 compared to finasteride group, increased the expressions while decreased the expression of DKK-1. Tissue histological analysis shows that administration of ginsenoside F2 promoted hair growth as compared to finasteride, increase in the number of hair follicles, thickness of the epidermis, and follicles of the anagen phase [43]. Heon-Sub Shin conclude that ginsenoside F2 might be a potential new therapeutic compound for anagen induction and hair growth through the Wnt signal pathway [43]. In another study by Matsuda et al., ginsenosides Rg3 and Rb1 [63] extracted from red ginseng stimulates hair growth activity in an organ culture of mouse vibrissa follicles. No detailed explanations are given in this paper about the mechanism of hair growth, but the results presented by Matsuda et al. [63] indicated that Ginseng Radix possesses hair growth promoting activity.
\n\n
Growth factors and cytokines have been proved to influence hair follicle development or cycling [65] overexpression and/or secretion of Cytokines, such as interleukins (ILs) and interferons (IFN), cause skin inflammation, TGF beta 1 partially inhibited hair growth and EGF, TNF alpha and IL-1 beta completely abrogated it [66] There is an aberrant expression pattern of cytokines in alopecia areata hair follicles.
\nThe presence of CD8+ T cells and NKG2D+ cells around the peri-bulbar area of the affected hair follicles [67] and upregulation of several ILs, such as IL-2, IL-7, IL-15, and IL-21, and IFN-γ leads to immune activation area where’re main suppressed natural killer (NK) cells [68] and is defined as immune-tolerated area. Loss of immune tolerance [68] or immune activation [67], leads to hair-follicle dystrophy and acceleration of the catagen phase [9] by the activation of a cytotoxic cluster of differentiation 8-positive (CD8+) and NK group 2D-positive (NKG2D+) T cells. In alopecia Areata (AA) are found more CD57 − CD16+ NK cells and there is a association between NK cells and the collapse of HF-IP (immune privilege) while normal human scalp skin—that indeed there is no sign of an NK attack on normal anagen VI HFs [69].
\nPhosphorylate Stat3 in the Janus Kinase (JAK)/Signal transducer and activator of transcription-3 (STAT3) pathway regulate the activation of CD8+ and the NKG2D+ CD8+ T cells [70]. The inhibition of the upstream pathway JAK appears as a plausible target for developing a therapy for hair loss [67]. In fact, a number of JAK inhibitors, such as tofacitinib, ruxolitinib, baricitinib, CTP-543, PF-06651600 and PF-06700841 are in the progress of developing a therapy for alopecia [71, 72] more often in alopecia areata a common form of non-scarring hair loss that usually starts abruptly with a very high psychological impact [73], it is a T-cell-mediated disease which produces circular patches of non-scarring hair loss and nail dystrophy [72].
\nGinsenoside Rk1 inhibited the lipopolysaccharide- stimulated phosphorylation of JAK2 and STAT3 in murine macrophage cells [74] and Ginsenoside 20(S)-Rh2 exerts anti-cancer activity through targeting IL-6-induced JAK2/STAT3 [75]. Topical application of ginsenoside F2 by inhibiting the production of IL-17 and ROS, ameliorated dermal inflammation skin [69]. In the pathogenesis of alopecia areata is believed to be an imbalance of inflammatory cytokines IL-17. Monoclonal antibodies against IL-17A leads to hair regrowth in human volunteers [76]. Treatment with
Ginseng may be a multipurpose natural medicine with an extended history of medical application throughout the globe, particularly in Eastern countries.
\nThe beneficial effects of Ginseng cover a good spectrum from immune to cardiovascular, cancer and sexual diseases. New advances in the science leads elucidate new pharmacological activity of the ginseng and its ginsenosides. There are some studies of the use of Ginseng in dermatology investigating its effects from molecular to physiological in a skin cancer, dermatitis, alopecia wound injury and of course hair loss because also ginseng and its ginsenosides regulate the expression and activity of major proteins involved in hair-cycling phases, so the medical use of ginseng is not only restricted to the improvement of general wellness, but also extended to the treatment of organ-specific pathological conditions, like hair.
\nGinseng and its metabolites are associate with the induction of anagen phase preventing hair lost and promoting hair growth although further studies should be done to elucidate and clarified the mechanisms by which ginseng and its metabolites regulate human hair health.
\nThe authors declare no conflict of interest.
\n Alopecia Areata Androgenetic Alopecia Follicular Unit United States Food and Drug Administration Dickkopf homolog 1 sonic hedgehog vascular endothelial growth factor transforming growth factor-beta matrix metalloproteinase extracellular signal-regulated protein kinase Janus-activated kinase protopanaxadiol protopanaxatriol compound K ultraviolet radiation reactive oxygen species linoleic acid β-sitosterol testosterone human hair-follicle dermal papillary cells red-ginseng extract hair follicle dermal papilla cells Gintonin-enriched fraction Korean Red Ginseng Dermal papillary cells NK group 2D-positive UL16-binding protein 3 glioma-associated oncogene homolog cluster of differentiation 8-positive interleukins interferons outer root sheath Signal transducer and activator of transcription-3 Wingless-type integration-site Gintonin-enriched fraction
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Heavy metals are known to be naturally occurring compounds, but anthropogenic activities introduce them in large quantities in different environmental compartments. This leads to the environment’s ability to foster life being reduced as human, animal, and plant health become threatened. This occurs due to bioaccumulation in the food chains as a result of the nondegradable state of the heavy metals. Remediation of heavy metals requires special attention to protect soil quality, air quality, water quality, human health, animal health, and all spheres as a collection. Developed physical and chemical heavy metal remediation technologies are demanding costs which are not feasible, time-consuming, and release additional waste to the environment. This chapter summarises the problems related to heavy metal pollution and various remediation technologies. A case study in South Africa mines were also used.",book:{id:"6534",slug:"heavy-metals",title:"Heavy Metals",fullTitle:"Heavy Metals"},signatures:"Vhahangwele Masindi and Khathutshelo L. Muedi",authors:[{id:"225304",title:"Dr.",name:"Vhahangwele",middleName:null,surname:"Masindi",slug:"vhahangwele-masindi",fullName:"Vhahangwele Masindi"},{id:"241403",title:"M.Sc.",name:"Khathutshelo",middleName:"Lilith",surname:"Muedi",slug:"khathutshelo-muedi",fullName:"Khathutshelo Muedi"}]},{id:"59905",title:"Synthesis of Silver Nanoparticles",slug:"synthesis-of-silver-nanoparticles",totalDownloads:6761,totalCrossrefCites:9,totalDimensionsCites:18,abstract:"Nanoparticles of noble metals, especially the silver nanoparticles, have been widely used in different fields of science. Their unique properties, which can be incorporated into biosensor materials, composite fibers, cosmetic products, antimicrobial applications, conducting materials and electronic components, make them a very important subject to be studied by chemistry, biology, healthcare, electronic and other related branches. These unique properties depend upon size and shape of the silver nanoparticles. Different preparation methods have been reported for the synthesis of the silver nanoparticles, such as electron irradiation, laser ablation, chemical reduction, biological artificial methods, photochemical methods and microwave processing. 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The correlation between stability and reactivity of coordination compounds has been described in this chapter. This chapter also enlists the factors influencing the stability of metal complexes such as the nature of metal ions, ligands, bonding between metal ions and ligands, etc. In addition, the methods available for the determination of stability constants are given in detail.",book:{id:"9190",slug:"stability-and-applications-of-coordination-compounds",title:"Stability and Applications of Coordination Compounds",fullTitle:"Stability and Applications of Coordination Compounds"},signatures:"Senthilkumar Muthaiah, Anita Bhatia and Muthukumar Kannan",authors:null},{id:"60518",title:"Synthetic Methods for Titanium Dioxide Nanoparticles: A Review",slug:"synthetic-methods-for-titanium-dioxide-nanoparticles-a-review",totalDownloads:5149,totalCrossrefCites:26,totalDimensionsCites:50,abstract:"Titanium dioxide (TiO2) semiconductor nanoparticles are one kind of important and promising photocatalysts in photocatalysis because of their unique optical and electronic properties. Their properties, which are determined by the preparation method, are very crucial in photocatalysis. In this chapter, an overview was carried out on the different methods that are used or have been used to prepare titanium dioxide nanoparticles. There are various methods that can be used to synthesize TiO2 and the most commonly used methods include sol-gel process, chemical vapor deposition (CVD) and hydrothermal method among others. This review will focus on selected preparation methods of titanium dioxide photocatalyst.",book:{id:"6426",slug:"titanium-dioxide-material-for-a-sustainable-environment",title:"Titanium Dioxide",fullTitle:"Titanium Dioxide - Material for a Sustainable Environment"},signatures:"Pardon Nyamukamba, Omobola Okoh, Henry Mungondori,\nRaymond Taziwa and Simcelile Zinya",authors:[{id:"196100",title:"Dr.",name:"Raymond",middleName:null,surname:"Taziwa",slug:"raymond-taziwa",fullName:"Raymond Taziwa"},{id:"219920",title:"Prof.",name:"Omobola",middleName:null,surname:"Okoh",slug:"omobola-okoh",fullName:"Omobola Okoh"},{id:"226567",title:"Dr.",name:"Pardon",middleName:null,surname:"Nyamukamba",slug:"pardon-nyamukamba",fullName:"Pardon Nyamukamba"},{id:"239758",title:"Mr.",name:"Simcelile",middleName:null,surname:"Zinya",slug:"simcelile-zinya",fullName:"Simcelile Zinya"}]}],onlineFirstChaptersFilter:{topicId:"158",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:87,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:98,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:27,numberOfPublishedChapters:287,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:139,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:0,numberOfUpcomingTopics:2,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!1},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:10,numberOfPublishedChapters:103,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:0,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!1},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:11,numberOfOpenTopics:4,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. He is the founder of The IEEE IWOBI conference series and the president of its Steering Committee, as well as the founder of both the InnoEducaTIC and APPIS conference series. He is an evaluator of project proposals for the European Union (H2020), Medical Research Council (MRC, UK), Spanish Government (ANECA, Spain), Research National Agency (ANR, France), DAAD (Germany), Argentinian Government, and the Colombian Institutions. He has been a reviewer in different indexed international journals (<70) and conferences (<250) since 2001. 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He has (co)authored more than 150 publications in indexed journals, international conferences and book chapters, 1 book (in Greek), 3 edited books, and 5 journal special issues. His publications have more than 2100 citations with h-index 27 (GoogleScholar). His research interests include computer/machine vision, machine learning, pattern recognition, computational intelligence. \nDr. Papakostas served as a reviewer in numerous journals, as a program\ncommittee member in international conferences and he is a member of the IAENG, MIR Labs, EUCogIII, INSTICC and the Technical Chamber of Greece (TEE).",institutionString:null,institution:{name:"International Hellenic University",institutionURL:null,country:{name:"Greece"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"1177",title:"Prof.",name:"Antonio",middleName:"J. 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