目的观察细胞外信号调节激酶1/2(ERK1/2)在血管紧张素Ⅱ诱导的内皮细胞中不同时点的表达变化,为阐明血管内皮细胞凋亡对动脉粥样硬化的诊治具有重要意义。方法制备血管紧张素ⅡRPMI1640培养液(10-6mol/L)培养人脐静脉内皮细胞,采用四甲基偶氮唑蓝比色法测定内皮细胞存活率,通过AnnexinV-FITC/PI双染流式细胞仪检测细胞凋亡率、Hochest33258荧光染色观察凋亡细胞形态学的变化,利用RT-PCR法分析凋亡调控基因Bcl-2、Bax mRNA表达变化,Western-Blot测定磷酸化ERK1/2水平。结果血管紧张素Ⅱ诱导内皮细胞的凋亡率明显高于对照组(P<0.01),与对照组相比,Bcl-2 mRNA表达呈持续性降低;Bcl-2/Bax比值下降,ERK1/2磷酸化水平于12 h明显增加,18 h达到高峰(P<0.01),24 h下降至稳定,总ERK1/2蛋白水平无明显变化。结论 ERK1/2信号转导途径参与血管紧张素Ⅱ诱导内皮细胞的凋亡发生、发展过程,并可能通过调控内皮细胞Bcl-2/Bax比值来实现。 Objective To observe the expression changes of extracellular signal - regulated kinase 1/2 (ERK1 / 2) in angiotensin Ⅱ induced endothelial cells at different time points. It is important to clarify the apoptosis of vascular endothelial cells in the diagnosis and treatment of atherosclerosis. Methods Human umbilical vein endothelial cells were cultured with RPMI1640 medium (10-6mol / L). The survival rate of endothelial cells was measured by MTT assay. The viability of endothelial cells was detected by Annexin V-FITC / PI double staining flow cytometry The apoptotic rate was detected by Hoechst 33258 staining. The morphological changes of apoptotic cells were observed by RT-PCR. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR. The phosphorylated ERK1 / 2 levels were detected by Western-Blot. Results The apoptosis rate of endothelial cells induced by angiotensin Ⅱ was significantly higher than that of the control group (P <0.01). Compared with the control group, the expression of Bcl-2 mRNA was decreased continuously. The ratio of Bcl-2 / Phosphorylation increased significantly at 12 h, peaked at 18 h (P <0.01), decreased to stable at 24 h, and showed no significant change in total ERK1 / 2 protein levels. Conclusion ERK1 / 2 signal transduction pathway is involved in angiotensin Ⅱ-induced endothelial cell apoptosis and development, and may be through the regulation of endothelial cell Bcl-2 / Bax ratio.