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Editorial
. 2009 Dec;23(6):425-9.
doi: 10.1007/s10557-009-6209-0.

Resveratrol: a multifunctional compound improving endothelial function. Editorial to: "Resveratrol supplementation gender independently improves endothelial reactivity and suppresses superoxide production in healthy rats" by S. Soylemez et al

Editorial

Resveratrol: a multifunctional compound improving endothelial function. Editorial to: "Resveratrol supplementation gender independently improves endothelial reactivity and suppresses superoxide production in healthy rats" by S. Soylemez et al

Huige Li et al. Cardiovasc Drugs Ther. 2009 Dec.

Erratum in

  • Cardiovasc Drugs Ther. 2010 Feb;24(1):91

Abstract

The red wine polyphenol resveratrol boosts endothelium-dependent and -independent vasorelaxations. The improvement of endothelial function by resveratrol is largely attributable to nitric oxide (NO) derived from endothelial NO synthase (eNOS). By stimulating eNOS expression, eNOS phosphorylation and eNOS deacetylation, resveratrol enhances endothelial NO production. By upregulating antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and suppressing the expression and activity of NADPH oxidases, resveratrol inhibits superoxide-mediated NO inactivation. Some resveratrol effects are mediated by sirtuin 1 (SIRT1) or estrogen receptors, respectively.

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Figures

Fig. 1
Fig. 1
Mechanisms of resveratrol-induced improvement of vascular function. Resveratrol induces vasorelaxation through both endothelium-dependent and -independent mechanisms. Resveratrol increases endothelial NO production by SIRT1-dependent eNOS upregulation, SIRT1-dependent eNOS deacetylation and estrogen receptor ERα-dependent, ERK1/2-mediated eNOS phosphorylation. By decreasing the expression and activity of vascular NADPH oxidases (NOX) and enhancing the expression of superoxide dismutases (SOD), catalase and glutathione peroxidases, resveratrol decreases superoxide-mediated NO inactivation. The resulting elevation in NO bioactivity is likely to mediate the endothelium-dependent relaxation. Ion channels seem to be involved in the endothelium-independent effects of resveratrol

Comment on

References

    1. Baur JA, Sinclair DA. Therapeutic potential of resveratrol: the in vivo evidence. Nat Rev Drug Discov. 2006;5:493–506. doi: 10.1038/nrd2060. - DOI - PubMed
    1. Bradamante S, Barenghi L, Villa A. Cardiovascular protective effects of resveratrol. Cardiovasc Drug Rev. 2004;22:169–188. - PubMed
    1. Opie LH, Lecour S. The red wine hypothesis: from concepts to protective signaling molecules. Eur Heart J. 2007;28:1683–1693. doi: 10.1093/eurheartj/ehm149. - DOI - PubMed
    1. Vingtdeux V, Dreses-Werringloer U, Zhao H, Davies P, Marambaud P. Therapeutic potential of resveratrol in Alzheimer’s disease. BMC Neurosci. 2008;9:S6. doi: 10.1186/1471-2202-9-S2-S6. - DOI - PMC - PubMed
    1. Chen CK, Pace-Asciak CR. Vasorelaxing activity of resveratrol and quercetin in isolated rat aorta. Gen Pharmacol. 1996;27:363–366. - PubMed