Effects And Mechanisms Of Curcumin Regulated SIRT1 Protect Against Human Umbilical Vein Endothelial Cell Senescence

MaterialEndothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. Curcumin, a kind of natural phenols, possesses antioxidant and anti-inflammatory properties. However, the effect of curcumin on endothelial senescence is unclear. This study was to explore the effect of curcumin on hydrogen peroxide (H2O2)-induced endothelial premature senescence and the mechanisms were involved.MethodsHuman umbilical vein endothelial cells (HUVECs) were cultured and the premature senescence was induced with 100?M H2O2 with or without pretreatment of curcumin. Senescence associated ?-galactosidase (SA-?G) assay was performed to evaluate cellular senescence and cell cycle analysis was studied with flow cytometry. The protein levels of SIRT1, p21, p-eNOS (Ser1177) and eNOS were detected using Western blotting, and the level of nitric oxide (NO) in culture medium was also detected. SIRT1 siRNA was used to explore the involvement of SIRT1 in the effect of curcumin on H2O2-induced premature senescence.ResultsCurcumin significantly attenuated H2O2-induced premature senescence in HUVECs, which was evidenced by improved cell viability and a decreased percentage of SA-?G positive cells (all p<0.05). Western blotting analyses showed that treatment of H2O2 down-regulated the phosphorylation of eNOS, decreased the level of NO in culture medium, and increased the expression of p21, while pretreatment with curcumin reversed these effects (all p<0.05). Pretreatment of curcumin could significantly increase the expression of SIRT1 (p<0.05) and inhibition of SIRT1 with SIRT1 siRNA could abrogate the protective effect of curcumin on H2O2-induced premature senescence (p>0.05).ConclusionsIn the present study, we found that curcumin could increase the expression of SIRT1 in H2O2-treated HUVECs and silencing of SIRT1 abolishes the protective effect of curcumin.