Resveratrol Increases Vascular Oxidative Stress Resistance.
From: Department of Physiology, New York Medical College, Valhalla, NY 10595, USA. zoltan_ungvari@nymc.edu
American journal of physiology. Heart and circulatory physiology
- Publish Date: May 2007
- ISSN: 0363-6135
- Volume: 292
- Issue: 5
- Pages: H2417-24
- Medium: Print
- Language: English
- Citation (JAMA): Ungvari Zoltan, Orosz Zsuzsanna, Rivera Aracelie, et al. Resveratrol Increases Vascular Oxidative Stress Resistance.. Am. J. Physiol. Heart Circ. Physiol. May 2007;292:H2417-24
Abstract
Epidemiological studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease. However, the mechanisms by which resveratrol exerts its vasculoprotective effects are not completely understood. Because oxidative stress and endothelial cell injury play a critical role in vascular aging and atherogenesis, we evaluated whether resveratrol inhibits oxidative stress-induced endothelial apoptosis. We found that oxidized LDL and TNF-alpha elicited significant increases in caspase-3/7 activity in endothelial cells and cultured rat aortas, which were prevented by resveratrol pretreatment (10(-6)-10(-4) mol/l). The protective effect of resveratrol was attenuated by inhibition of glutathione peroxidase and heme oxygenase-1, suggesting a role for antioxidant systems in the antiapoptotic action of resveratrol. Indeed, resveratrol treatment protected cultured aortic segments and/or endothelial cells against increases in intracellular H(2)O(2) levels and H(2)O(2)-mediated apoptotic cell death induced by oxidative stressors (exogenous H(2)O(2), paraquat, and UV light). Resveratrol treatment also attenuated UV-induced DNA damage (comet assay). Resveratrol treatment upregulated the expression of glutathione peroxidase, catalase, and heme oxygenase-1 in cultured arteries, whereas it had no significant effect on the expression of SOD isoforms. Resveratrol also effectively scavenged H(2)O(2) in vitro. Thus resveratrol seems to increase vascular oxidative stress resistance by scavenging H(2)O(2) and preventing oxidative stress-induced endothelial cell death. We propose that the antioxidant and antiapoptotic effects of resveratrol, together with its previously described anti-inflammatory actions, are responsible, at least in part, for its cardioprotective effects.
Mesh Headings (Keywords): Animals, Antioxidants, Apoptosis, Cells, Cultured, Dose-Response Relationship, Drug, Endothelial Cells, Hydrogen Peroxide, Oxidative Stress, Rats, Reactive Oxygen Species, Stilbenes
Check for Full Text / PubMed Unique Identifier (PMID): 17220179
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.