Atorvastatin Delay the Senescence of Vascular Endothelial Cell Induced by AngiotensinII Through Regulating the Expression of Bcl-2/Bax Protein

Aim To explore the effects of Atorvastatin on the senescence in human umbilical vein endothelial cells(HUVEC) induced by angiotensinⅡ(AngⅡ) and to study its potential molecular mechanism. Method The HUVEC were cultured in vitro and divided into 3 groups,the control group,AngⅡgroup(stimulated and intervened by AngⅡ10-6mol/L for 48 h),Atorvastatin group(10-3mol/L Atorvastatin was added to cell 1 h before 10-6mol/L AngⅡ).β-Gal stain and cell cycle analysis were used to identify cell aging status;and the expression of apoptosis-association genes Bcl-2 and Bax were detected by immunocytochemistry,and Western blot. Results AngⅡ stimulation enhanced the positive cell number of β-gal stained HUVEC,depressed cell proliferation.The AngⅡ group inhibited the expression of Bcl-2 protein and increased the expression of Bax protein compared with the Atorvastatin group markedly(P0.05),Bcl-2/Bax was decreased significantly(P0.05) in the AngⅡgroup.The Atorvastatin group increased the expression of Bcl-2 protein and decreased the expression of Bax protein compared with the AngⅡ group evidently(P0.05),Bcl-2/Bax was increased significantly(P0.05) in the Atorvastatin group. Conclusions Atorvastatin probably delay the senescence of vascular endothelial cell induced by AngⅡ through regulating the expression of Bcl-2/Bax protein.