血管紧张素Ⅱ诱导培养的牛脑微血管内皮细胞凋亡及其机制

目的　研究AngⅡ对牛脑微血管内皮细胞(BCMEC)有无诱导凋亡的作用。方法　利用流式细胞仪和透射电子显微镜检测体外培养的BCMEC凋亡。结果　流式细胞术显示AngⅡ (0 .0 1～ 10 μmol·L- 1)呈浓度依赖性诱导BCMEC凋亡。 10 μmol·L- 1AngⅡ诱导的BCMEC凋亡不能被 10 0 μmol·L- 1AT1受体拮抗剂氯沙坦所抑制 ,而能被 15 0kU·L- 1超氧化物歧化酶所部分抑制。BCMEC经 10 μmol·L- 1AngⅡ刺激 18h后 ,呈现胞浆浓缩、染色质凝集、核碎裂和凋亡小体形成等凋亡的超微结构变化。结论AngⅡ能诱导BCMEC凋亡 ,其机制可能与其刺激BCMEC产生的氧自由基有关。AngⅡ诱导脑血管内皮细胞凋亡可能是其参与脑血管疾病的机制之一

Apoptosis and its mechanism of bovine cerebral microvessel endothelial cells induced by angiotensin Ⅱ

AIM To study if angiotensin Ⅱ(AngⅡ) induces apoptosis of bovine cerebral microvessel endothelial cells(BCMEC). METHODS The primary cultured BCMEC were incubated with AngⅡ for 18 h, apoptosis was evaluated by flow cytometry and electron transmission micros copy. RESULTS Flow cytometry revealed that AngⅡ 0.01－10 μmol·L^-1 induced BCMEC apoptosis in ａ dose-dependent manner. The proapoptotic effect of AngⅡ at 10 μmol·L^-1 was significantly attenuated by 150 kU·L^-1 superoxide dismutase, but not by 100 μmol·L^-1 losartan, the AT₁ receptor antagonist. After treatment with AngⅡ for 18 h, BCMEC showed ultrastructural changes of apoptosis including shrinkage, condensation of nuclear chromatin, fragmentation of nuclei and formation of apoptotic body. CONCL USIONAngⅡ can induce BCMEC apoptosis by a mechanism involving oxygen-free radicals production.