CAJ | 학술논문

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。
목적：관찰혈관긴장소Ⅱ치내피세포（HUVECs）조망적작용병탐토기가능궤제。방법체외배양인제정맥내피세포주ECV-304，이혈관긴장소Ⅱ（AngⅡ）제비혈관내피세포손상모형，ERK1/2억제제PD98059진행간예。류식세포의측정내피세포조망솔；면역인적법측정포외신호조절격매（ERK1/2）적표체。결과 AngⅡ가도치내피세포조망；병가명현촉진내피세포ERK1/2표체；PD98059가강저AngⅡ소치내피세포조망솔。결론 AngⅡ가유도적HUVECs조망，촉진ERK1/2표체가능시작용궤제지일。
Objective To clarify the proapoptotic effect and mechanism of Angiotensin Ⅱ (AngⅡ) on cultured HUVECs. Methods Human umbilicalVECs (ECV304) were used. The vascular endothelial injur ed cell model was prepared using An-giotensinⅡ. 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 AngⅡ. PD98059 may reduce apoptosis ratio of endothelial cells induced by AngⅡ. Conclusions AngⅡcan induce VEC apoptosis,which might be re-lated to the expression of ERK1/2.