Part of the book: Advances in the Preclinical Study of Ischemic Stroke
Stroke-prone spontaneously hypertensive (SHRSP) rats develop severe hypertension, and more than 95% of them die of cerebral stroke. Cerebral ischemia or hypoxia and/or subsequent oxygen reperfusion strongly induces neuronal damage in SHRSP rats. The biochemical features of brain cells such as neuronal cells and astrocytes of SHRSP rats might contribute to the strong tendency of SHRSP rats to suffer strokes. In SHRSP rats, the production of hydroxyl radicals was strongly elevated after reperfusion. Neuronal expression of thioredoxin (Txn1) and Bcl2 genes was significantly reduced in SHRSP rats compared with Wistar Kyoto (WKY) rats. In SHRSP rats, the susceptibility of neuronal cells to death is partly due to an insufficiency of mitochondrial redox regulation and a deficiency of the apoptosis-inhibitory protein Bcl-2. Antioxidant vitamin E may regulate the expression of redox and apoptosis-related proteins in neuronal damage. In astrocytes isolated from SHRSP rats, the cells’ proliferative ability and expression of vascular cell adhesion molecule-1 (VCAM-1) and high-mobility group box 1 (HMGB1) are strongly increased compared with those in the WKY rat strain. Astrocytic lactate production, an energy source for neuronal cells, was reduced in SHRSP rats in comparison with the WKY rat strain. SHRSP astrocytes reduced their production of glial cell line–derived neurotrophic factor (GDNF) and l-serine compared to WKY astrocytes during hypoxia and reoxygenation (H/R). Furthermore, sphingosine-1-phosphate (S1P) reduced the expression of GDNF in primary SHRSP rat astrocytes. On the other hand, production of l-serine and the expression of alanine/serine/cysteine/threonine transporter (ASCT1) were lower in SHRSP than in WKY rat astrocytes after exposure to arginine vasopressin (AVP). In this chapter, we describe the neuronal vulnerabilities and astrocytic dysfunctions of SHRSP rats induced by cerebral ischemia.
Part of the book: Ischemic Stroke
Regular consumption of fruits and vegetables can help reduce the risk for cardiovascular disease (CVD) and its associated mortality. A diet rich in fruits and vegetables is thought to have cardioprotective effects, but the specific components of these foods that provide this protection are unclear. Antioxidants such as vitamin C, carotenoids, and polyphenols in fruits and vegetables likely contribute to the reduction in risk of CVD by minimizing cholesterol oxidation in blood vessel walls. Meanwhile, cardioprotective effects afforded by the carotenoids lycopene, α-carotene, β-carotene, β-cryptoxanthin, lutein, and zeaxanthin have been reported in many studies. Carotenoids are naturally occurring fat-soluble pigments that are present at high levels in tomatoes and carrots. Carotenoids play an important role in staving off atherosclerosis via antioxidant activities that reduce lipid peroxidation in low-density lipoproteins. Lycopene reduces endothelin-1 gene expression by suppressing generation of reactive oxygen species and inducing heme oxygenase-1 expression in human endothelial cells. Thus, carotenoids may mitigate endothelial dysfunction by promoting direct antioxidative effects and inducing expression of several genes. Structural and functional differences among carotenoids may explain their unique biologic activities. In this review, the roles of carotenoids in relation to their influence on vascular endothelial functions and cardioprotective effects are discussed.
Part of the book: Carotenoids