论文部分内容阅读
研究了 AT2 受体在血管紧张素 II (Ang II)及 2型血管紧张素 II受体 (AT2 )兴奋剂 CGP42 112 A作用下能否诱导人内皮细胞凋亡及其与半胱氨酰蛋白酶 (cystolic aspartatic proteases )之 Caspase-3的关系。结果显示 ,Ang II或 CGP42 112 A可以诱导人内皮细胞出现典型的细胞凋亡 ,凋亡细胞阳性率极显著高于阴性对照组 ,凋亡的相对强度与 Ang II呈现典型的剂量依赖关系。Caspase-3酶活性在 Ang II或 CGP42 112 A作用后有极显著的增加 ,而在用 Caspase-3抑制剂 DEVD-fmk后凋亡不能诱导。提示 AngII或 CGP42 112 A可以通过 AT2 受体诱导人内皮细胞凋亡 ,并且此凋亡是 Caspase-3依赖性的
We investigated whether AT2 receptor can induce apoptosis of human endothelial cells under the action of angiotensin II (Ang II) and type 2 angiotensin II receptor (AT2) agonist CGP42 112 A and its interaction with cysteinyl protease cystolic aspartatic proteases) of the Caspase-3 relationship. The results showed that Ang II or CGP42 112 A induced typical apoptosis in human endothelial cells. The positive rate of apoptotic cells was significantly higher than that of the negative control group. The relative intensity of apoptosis correlated with the typical dose-dependent relationship of Ang II. Caspase-3 activity increased significantly after Ang II or CGP42 112 A treatment, but not by DEVD-fmk Caspase-3 inhibitor. Suggesting AngII or CGP42 112 A can induce apoptosis in human endothelial cells via the AT2 receptor and this apoptosis is Caspase-3-dependent