摘要
目的研究血管紧张素Ⅱ(AngⅡ)诱导细胞凋亡的机制。方法健康胎儿脐静脉内皮细胞培养至第3代,用不同浓度AngⅡ作用18h,用TUNEL和ELISA检测AngⅡ能否诱导细胞凋亡及其量效关系;用RT-PCR检测bax和bcl-2的mRNA表达。结果AngⅡ与2型血管紧张素Ⅱ受体(AT2)激动剂CGP42112A一样可以诱导血管内皮细胞凋亡;并且凋亡强度与AngⅡ呈典型的剂量依赖关系。在AngⅡ与CGP4211A作用18h后,bax mRNA显著增加,bcl-2mRNA显著减少。结论AngⅡ通过在转录水平调节bax和bcl-2mRNA的表达,从而诱导血管内皮细胞凋亡。
Objective To study human endothelial apoptosis induced by angiotensin Ⅱ （Ang Ⅱ ） and its molecular mechanism. Methods Blood endotheliocytes isolated from healthy human infant umbilical vein were cultured to the third passage and incubated with Ang Ⅱ in various concentrations for 18 h. The apoptosis was detected by TUNEL and ELISA. The expression of bax and bcl-2 mRNA was determined by RT-PCR and densitometry. Results Ang Ⅱ, like AT2 receptor agonist CGP42112A, could induce the typical endothelial apoptosis in a dose-dependent manner. Apoptotic positive cell percentage in Ang Ⅱ treatment group was significantly higher than that in normal control group. The expression of bax mRNA was higher and that of bcl-2 mRNA lower in Ang Ⅱ or CGP42112A treatment group than in normal control group. Conclusion Ang Ⅱ triggered apoptosis of human blood endotheliocytes by up-regulating the expression of proapoptotic bax mRNA and down-regulating the expression of antiapoptotic bcl-2 mRNA.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2005年第6期727-729,共3页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
教育部留学回国人员科研启动基金资助项目(教外司留[2000]479)
