RESUMEN
AIM:To explore the role of Sirt1/eNOS signalling pathway in the protective effect of hydrogen sul-phide(H2S)against endothelial cell senescence induced by high glucose.METHODS:High glucose(33 mmol/L)was applied to induce senescence in primary human umbilical vein endothelial cells(HUVECs).The cell viability,the propor-tion of senescence-associated β-galactosidase(SA-β-Gal)positive cells and the plasminogen activator inhibitor 1(PAI-1) expression were detected to assess the senescence model.Mean while,Sirt1 siRNA was used to examine the effect of Sirt 1 on eNOS expression and the senescence-related parameters.RESULTS: Treatment of HUVECs with high glucose de-creased the cell viability slowly with a larger proportion of the cells stained with SA-β-Gal, and the protein expression of PAI-1 was dramatically increased.The increased cell viability,reduced SA-β-Gal positive cells and decreased protein ex-pression of PAI-1 were detected after sodium hydrosulfide(NaHS,100 μmol/L)treatment.Furthermore,NaHS treatment upregulated the protein expression of Sirt 1 and eNOS,and eventually increased the production of nitric oxide(NO).CON-CLUSION:Exogenous H2S modulates Sirt1/eNOS/NO pathway to prevent HUVECs against high glucose-induced senes-cence.