血管紧张素Ⅱ诱导人内皮细胞凋亡

The Apoptosis of Human Endothelium Induced by Angiotensin Ⅱ

为探讨血管紧张素 ( Ang )能否诱导人内皮细胞凋亡 ,将健康胎儿脐静脉内皮细胞培养至第 3代 ,用不同浓度 Ang 培养不同时间 ,用 TUNEL 和 EL ISA检测细胞凋亡 ,并检验 Caspase- 3酶活性变化。用 RT- PCR检测 Ang 受体 AT1 和 AT2 的 m RNA表达。发现 Ang 可以诱导出典型的凋亡 ,凋亡细胞阳性率极显著高于对照组 ,凋亡强度与 Ang 呈现剂量依赖关系。Caspase- 3酶活性在 Ang 作用后有极显著的增加。内皮细胞同时表达 AT1 和 AT2 的 m R-NA。结果表明 :Ang 经 AT1 或 (和 ) AT2 可以诱导人内皮细胞凋亡 ,并且是 Caspase- 3依赖性的。这一结果有助于阐明Ang 的致病机制。

To study whether Angiotensin Ⅱ (Ang Ⅱ) could induce apoptosis of human endothelium, the endothelium isolated from healthy human infant umbilical vein was cultured to the third passage. Then Ang Ⅱ was added into it in various concentrations and further cultured for different time periods. The apoptosis was identified by TUNEL and ELISA. The activity of Caspase-3 was assayed by spectrophotometry. The expression of AT 1 - and AT 2 -mRNA was detected by RT-PCR. It was found that Ang Ⅱ induced typical endothelial apoptosis. The apoptotic positive cell percentage and activity of Caspase-3 was significantly higher in the Ang Ⅱ treatment group than in the control group. The intensity of apoptosis was related with the Ang Ⅱ in a dose-dependent manner. In addition, the expression of AT 1-and AT 2 -mRNA was simultaneously observed in the endothelium. It was suggested that Ang Ⅱ could trigger apoptosis of human endothelium mediated by AT 1 or(and) AT 2 receptor and that apoptosis was dependent on the activation of Caspase-3, which might be helpful to explore the pathogenesis of Ang Ⅱ-related diseases.