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目的 研究AngⅡ诱导凋亡细胞内机制。方法 健康胎儿脐静脉内皮细胞培养至第三代,用不同浓度AngⅡ作用不同时间,用TUNEL和ELISA检测AngⅡ能否诱导凋亡及有否剂量依赖性;用RT—PCR检测bax的mRNA表达。结果 AngⅡ同AT2 受体激动剂CGP42 1 1 2A一样可以诱导内皮细胞凋亡;并且凋亡强度与AngⅡ成典型的剂量依赖关系。在AngⅡ与CGP42 1 1A作用1 8小时后,baxmRNA显著增加。结论 AngⅡ在转录水平上诱导baxmRNA高表达,使得Bax蛋白高表达,致Bax Bcl- 2比值极显著地增加,细胞内促凋亡因素占优势地位而诱发凋亡。
Objective To study the intracellular mechanism of Ang Ⅱ induced apoptosis. Methods Healthy fetal umbilical vein endothelial cells were cultured to the third generation. Different concentrations of AngⅡ were used for different time periods. TUNEL and ELISA were used to detect whether AngⅡ could induce apoptosis and dose-dependent manner. The mRNA expression of bax was detected by RT-PCR. Results AngⅡ could induce endothelial cell apoptosis in the same way as AT2 receptor agonist CGP42 1 1 2A; and the intensity of apoptosis was in a dose-dependent manner with AngⅡ. After AngⅡ and CGP42 1 1A were administered for 18 hours, bax mRNA was significantly increased. Conclusions AngⅡ induces the high expression of bax mRNA at the transcriptional level, which leads to the high expression of Bax protein. The ratio of Bax to Bcl-2 significantly increases, and the intracellular pro-apoptotic factors predominate to induce apoptosis.