中国病理生理杂志2018，Vol.34Issue(5)：893-898,6.DOI:10.3969/j.issn.1000-4718.2018.05.018
血管紧张素1-7通过Mas受体减轻血管紧张素Ⅱ所致人肾小球内皮细胞损伤
Angiotensin 1-7 attenuates angiotensin Ⅱ-induced human glomerular en-dothelial cell injury via Mas receptor
摘要
Abstract
AIM:To investigate the effect of angiotensin 1-7(Ang1-7)on the human glomerular endothelial cells(HGECs)injury induced by angiotensin Ⅱ(Ang Ⅱ)and its possible mechanism.METHODS: Cultured HGECs were divided into 6 groups randomly: control group, Ang Ⅱ group, Ang1-7 group, Ang Ⅱ +Ang1-7 group, Ang Ⅱ +Ang1-7+A779(an inhibitor of Mas receptor)group and A779 group.The apoptotic rate and reactive oxygen species (ROS)of HGECs were analyzed by flow cytometry and photographed by fluorescence microscopy.The levels of lactate de-hydrogenase(LDH),nitric oxide(NO),endothelin-1(ET-1),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α), transforming growth factor-β(TGF-β),monocyte chemoattractant protein-1(MCP-1)and intercellular adhesion molecule-1(ICAM-1)in the supernatant of cell cultures were measured.RESULTS:Compared with the control group,the apoptot-ic rate and the average fluorescence intensity of ROS were increased in the Ang Ⅱ group,IL-6,TNF-α,TGF-β,ICAM-1 and MCP-1 in cell supernatants were also increased in the Ang Ⅱ group(P<0.05).Compared with the Ang Ⅱ group,the apoptotic rate,ROS level, and the above inflammatory factors were decreased in Ang Ⅱ +Ang1-7 group(P<0.05). Compared with the Ang Ⅱ +Ang1-7 group,adding A779 increased the cell apoptotic rate,ROS production and the releases of the above inflammatory factors in cell supernatants(P<0.05).Compared with the Ang Ⅱ group,adding Ang1-7 inhibi-ted the LDH leakage, ET-1 secretion and promoted the release of NO in a dose-dependent manner(P<0.05).CON-CLUSION:Ang1-7 attenuates the HGECs injury induced by Ang Ⅱ by inhibiting the Mas receptor.关键词
人肾小球内皮细胞/血管紧张素1-7/血管紧张素Ⅱ/Mas受体/细胞凋亡Key words
Human glomerular endothelial cells/Angiotensin 1-7/Angiotensin Ⅱ/Mas receptor/Apoptosis分类
医药卫生引用本文复制引用
张晓翠,侯兆玉,张红利,邓芳..血管紧张素1-7通过Mas受体减轻血管紧张素Ⅱ所致人肾小球内皮细胞损伤[J].中国病理生理杂志,2018,34(5):893-898,6.基金项目
安徽省2017年公益性技术应用研究联动计划项目(No.1704f0804027) （No.1704f0804027）
