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J Appl Physiol (December 28, 2006). doi:10.1152/japplphysiol.00881.2006
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Submitted on August 9, 2006
Accepted on December 18, 2006

Resveratrol Attenuates OxLDL-stimulated NADPH Oxidase Activity and Protects Endothelial Cells from Oxidative Functional Damages

Shu-ER Chow1, Ya-Ching Hshu2, Jong Shyan Wang3, and Jan kan chen2*

1 Center of General Studies, Chang-Gung University, Tao-Yuan, Kwei-San, Taiwan - Republic of China
2 Department of physiology, College of Medicine,Chang Gung University, Tao-Yuan, United States
3 Graduate Institute of Rehabilitation Science, Chang Gung University, Kwei-Shan, United States

* To whom correspondence should be addressed. E-mail: jkc508{at}mail.cgu.edu.tw.

Trans-Resveratrol (RSV) has been shown to have cardioprotective effect during ischemia reperfusion through reactive oxygen species (ROS) scavenging activity. Elevated ROS has been implicated in the initiation and progression of atherosclerosis. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of vascular ROS formation. In the present study, we show that exposure of vascular endothelial cell (EC) to oxLDL results in elevations of NOX activity and cellular ROS levels. The oxLDL effects are effectively suppressed by RSV or astringinin (AST), either before or after oxLDL exposure. In this study, we show that RSV/AST treatment appears to suppress NOX activity by reducing the membrane association of gp91phox and Rac1, two protein species required for the assembly of active NOX complex. Exposure to RSV or AST protects EC from oxidative functional damages, including antiplatelet activity and mononucleocyte adhesion. In addition, angiotensin-II induced NOX activation is also attenuated. These results suggest that RSV/AST protect EC from oxLDL-induced oxidative stress by both direct ROS scavenging and inhibition of NOX activity.




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