血管紧张素Ⅱ通过ERK1/2信号通路诱导脐静脉内皮细胞凋亡  

Proapoptotic effect of angiotensin Ⅱon cultured endothelial cell via extracellular signal regulated kinases1/2

作　　者：邱宇安[1] 黄绍烈[2] 陈火国[3] 李丽红[3] 靳文剑[3] 余洁丽 

机构地区：[1]江西省肿瘤医院重症医学科,南昌330029 [2]南昌大学第一附属医院心内科,南昌330006 [3]江西省肿瘤医院内4科,南昌330029

出　　处：《江西医药》2015年第9期881-883,共3页Jiangxi Medical Journal

基　　金：江西省卫生厅中医药基金项目(2011A061)

摘　　要：目的观察血管紧张素Ⅱ致内皮细胞(HUVECs)凋亡的作用并探讨其可能机制。方法体外培养人脐静脉内皮细胞株ECV-304,以血管紧张素Ⅱ(AngⅡ)制备血管内皮细胞损伤模型,ERK1/2抑制剂PD98059进行干预。流式细胞仪测定内皮细胞凋亡率;免疫印迹法测定胞外信号调节激酶(ERK1/2)的表达。结果 AngⅡ可导致内皮细胞凋亡;并可明显促进内皮细胞ERK1/2表达;PD98059可降低AngⅡ所致内皮细胞凋亡率。结论 AngⅡ可诱导的HUVECs凋亡,促进ERK1/2表达可能是作用机制之一。Objective To clarify the proapoptotic effect and mechanism of Angiotensin Ⅱ（Ang Ⅱ） on cultured HUVECs.Methods Human umbilical VECs（ECV304） were used. The vascular endothelial injur ed cell model was prepared using AngiotensinⅡ. Flow cytometry was used to measure the apoptosis ratio. The ERK1/2 activity in VECs was detected by Western blot.Results VEC apoptosis was induced by AngⅡ. The ERK1/2 activity was increased after the exposure to Ang Ⅱ. PD98059 may reduce apoptosis ratio of endothelial cells induced by AngⅡ. Conclusions AngⅡcan induce VEC apoptosis,which might be related to the expression of ERK1/2.

关 键 词：血管紧张素Ⅱ ERK1/2 内皮细胞 凋亡 

分 类 号：R363[医药卫生—病理学]