Crimson wine polyphenols may preserve endothelial role during aging. Endothelial cell senescence enhances historic period-related endothelial dysfunction. We investigated whether RWE (reddish vino excerpt) prevents oxidative-stress-induced senescence in HUVECs (human umbilical-vein endothelial cells). Senescence was induced past exposing HUVECs to tBHP (t-butylhydroperoxide), and quantified by senescence-associated β-galactosidase staining. RWE (0–50 μg/ml) concentration dependently decreased senescence past maximally 33±7.i%. RWE prevented the senescence-associated increase in p21 protein expression, inhibited tBHP-induced Deoxyribonucleic acid damage of endothelial cells and induced relaxation of PCAs (porcine coronary arteries). Inhibition of SIRT1 (sirtuin 1) by sirtinol partially reversed the result of RWE on tBHP-induced senescence, whereas both the NOS (nitric oxide synthase) inhibitor Fifty-NMMA (N Yard-monomethyl-50-arginine) and the COX (cyclo-oxygenase) inhibitor indomethacin fully inhibited it. Furthermore, incubation of HUVECs with RWE increased eNOS (endothelial NOS) and COX-2 mRNA levels too as phosphorylation of eNOS at Ser1177. RWE protects endothelial cells from tBHP-induced senescence. NO and COX-2, in addition to activation of SIRT1, play a disquisitional role in the inhibition of senescence induction in man endothelial cells by RWE.

© The Authors Periodical compilation © 2012 Biochemical Society

2012

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