Plant polyphenols are dietary components that exert a variety of biochemical and pharmacological effects. Recently, considerable interest has been focused on polyphenols because of their antioxidant, anti-inflammatory, and antiproliferative activities. Oxidative stress is thought to be a key event in the pathogenesis of cerebral ischemia. Overproduction of reactive oxygen species during ischemia/reperfusion could cause an imbalance between oxidative and antioxidative processes. Reactive oxygen species can damage lipids, proteins, and nucleic acids, thereby inducing apoptosis or necrosis. There is increasing evidence supporting the hypothesis that plant polyphenols can provide protection against neurodegenerative changes associated with cerebral ischemia. This article reviews the neuroprotective effects of plant extracts and their constituents that have been used in animal models of cerebral ischemia. The use of polyphenols as therapeutic agents in stroke has been suggested.

Endothelial cells (ECs) play a role in the optimal function of blood vessels. When endothelial function becomes dysregulated, the risk of developing atherosclerosis increases. Specifically, upregulation of adhesion molecule expression on ECs promotes the movement of leukocytes, particularly monocytes, into the vessel wall. Here, monocytes differentiate into macrophages and may become foam cells, contributing to the initiation and progression of an atherosclerotic plaque. The ability of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) to influence the expression of adhesion molecules by ECs and to modulate leukocyte-endothelial adhesion has been studied in cell culture using various types of ECs, in animal feeding studies and in human trials; the latter have tended to evaluate soluble forms of adhesion molecules that circulate in the bloodstream. These studies indicate that n-3 PUFAs (both eicosapentaenoic acid and docosahexaenoic acid) can decrease the expression of key adhesion molecules, such as vascular cell adhesion molecule 1, by ECs and that this results in decreased adhesive interactions between leukocytes and ECs. These findings suggest that n-3 PUFAs may lower leukocyte infiltration into the vascular wall, which could contribute to reduced atherosclerosis and lowered risk of cardiovascular disease.

Yusof M, Kamada K, Kalogeris T, Gaskin FS, Korthuis RJ. Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO-and p38 MAPK-dependent mechanism.

Gaskin FS, Kamada K, Yusof M, Korthuis RJ. 5Ј-AMP-activated protein kinase activation prevents postischemic leukocyte-endothelial cell adhesive interactions.