AimTo investigate the role of Valsartan on Angiotensin Ⅱ(AngⅡ)-induced senescence of human umbilical endothelial cell senescence and gene expression of p16INK4a.MethodsHUVEC were cultured in vitro and intervened by AngⅡ(10-6mol/L) and Valsartan(AngⅡ type 1 receptor blocker).HUVEC were divided into 3 groups, the control group, AngⅡ group, Valsartan group.β-gal staining was used to identify cell aging status.Flow cytometry was used for analyzing the cell cycle changes; The positive cell rate of p16INK4a was detected by immunocytochemical staining, and the expressions of p16INK4a protein were determined by Western blot.ResultsCompared with the control cells, the positive cell number of β-gal staining was significantly higher in AngⅡ-induced cells 81.24%±6.46%; the cell cycle was at G0-G1 88.36%±6.45%. In Valsartan group, p16INK4a protein expression decreased evidently (p<0.05) compared to that in the AngⅡ group, which suggests that p16INK4a activity plays an important role in regulating vascular endothelial cell senescence lifespan in vitro.ConclusionCell Endothelial cell senescence is induced by AngⅡ.One of its molecular mechanisms might be associated with increasing the expression level of p16INK4a in aging cell, and then up-regulating the amount of cells blocking in G1 phase of cell cycle.Valsartan could antagonize the process effectively and delay endothelial cell aging significantly.