AimTo investigate the effects of angiotensinⅡ (AngⅡ) on apoptosis, and phosphorylation of p38 mitogen-activated protein kinase in endothelial cell, and its possible action mechanism.MethodHuman umbilical vein endothelial cells (HUVEC) were cultured in vitro and intervened by AngⅡ.HUVEC were divided into control group and AngⅡ group (stimulated by AngⅡ10－6 mol/L for 24 h), morphologic changes and percentage of apoptosis were assayed with acridine orange fluorescence staining.The early stage apoptosis was detected by flow cytometery with Annexin V-FITC/PI double staining.The expression of apoptosis-association gene Bcl-2 was detected by RT-PCR and Western blotting at different time points.By means of Western blotting, the activation of p38MAPK was observed at different time points.Results10－6 mol/L AngⅡ stimulated cell apoptosis.The percentage of apoptotic cells in AngⅡ-stimulated cells was significantly increased compared to that in the control cells (32.76%±2.98% vs 2.14%±0.36%, p<0.01) by using acridine orange fluorescence staining.The early-metaphase apoptotic rate was significantly increased in AngⅡ-stimulated cells compared to the control cells (37.4%±1.6% vs 10.2%±1.8%, p<0.01) by Annexin V-FITC/PI double staining flow cytometry.Bcl-2 mRNA and protein expression decreased markedly (p<0.05), the activation of p38MAPK began to increase and reach the peak at 18 h (p<0.01).ConclusionsCell apoptosis is possibly an impor-tant factor for atherosclerosis.One of its molecular mechanisms might be associated with decreasing the expression level of Bcl-2.There is a probability that activated p38MAPK signal pathway is involved in the process of pathologic and physiologic reaction in the apoptosis of endothelial cell induced by AngⅡ.