中国动脉硬化杂志2017，Vol.25Issue(10)：989-996,8.
血管紧张素(1-7)/Mas受体轴通过调控ATP敏感性钾通道对抗高糖引起的人脐静脉内皮细胞损伤
Angiotensin(1-7)/Mas receptor axis protects human umbilical vein endothelial cells against high glucose-induced injury by modulating ATP-sensitive K+ channels
摘要
Abstract
Aim To investigate whether angiotensin (1-7) [Ang (1-7)]/Mas receptor axis protects human umbilical vein endothelial cells (HUVEC) against high glucose (HG)-induced injury by modulating ATP-sensitive K+ channels (KATP channels).Methods Human umbilical vein endothelial cells were exposed to 40 mmol/L glucose to establish a model of HG-induced insults.The expression level of KATP channel protein was determined by Western blot,CCK-8 assay was used to test the cell viability,lactate dehydrogenase (LDH) activity in the culture medium was measured with commercial kits,Hoechst33258 staining was used to assess the number of apoptotic cells followed by photofluorography,the intracellular generation of reactive oxygen species (ROS) was measured by 2',7'-dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography,mitochondrial membrane potential (MMP) was detected by Rhodamine123 staining followed by photofluorography,the secretion levels of interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by ELISA.Results Human umbilical vein endothelial cells were treated with 40 mmol/L glucose for 1 ～ 24 h,respectively.After human umbilical vein endothelial cells were exposed to HG for 3 h,the level of KATP channelprotein decreased in a time-dependent manner,reaching the maximum decrease at the 24 h point.Co-treatment of the cells with 20 μmol/L Ang(1-7) and HG for 24 h ameliorated the down-regulation of KATp channel protein induced by HG.In addition,co-treatment of the cells with 20 μmol/L Ang(1-7) and HG or pre-treatment of the cells with 100 μmol/L pinacidil (a KATP channel opener) antagonized HG-induced injuries,evidenced by an increase in cell viability,a decrease in the activity of LDH,apoptotic cell number,ROS generation,MMP loss as well as the secretion levels of IL-1β and TNF-α.Co-treatment with 10 μmol/L A-779 (an inhibitor of Mas receptor) and HG or pre-treatment or 1 mmol/L glibenclamide (a KATP channel blocker) attenuated the above protective effects of Ang (1-7).Conclusion Ang (1-7) /Mas receptor axis protects human umbilical vein endothelial cells against HG-induced injury by modulating KATP channels.关键词
血管紧张素(1-7)/Mas受体轴/ATP敏感性钾通道/高糖/人脐静脉内皮细胞/细胞损伤Key words
Angiotensin (1-7)/Mas receptor axis/ATP-sensitive K+ channels/High glucose/Human umbilical vein endothelial cells/Cell injury分类
医药卫生引用本文复制引用
梁伟杰,陈君,余盛龙,陈美姬,林佳琼,吴文..血管紧张素(1-7)/Mas受体轴通过调控ATP敏感性钾通道对抗高糖引起的人脐静脉内皮细胞损伤[J].中国动脉硬化杂志,2017,25(10):989-996,8.基金项目
广东省自然科学基金项目(2015A030313872) （2015A030313872）
番禺区科技计划项目(2015-Z03-57) （2015-Z03-57）
番禺区中心医院硕博士科研基金项目(2015-S-02) （2015-S-02）
番禺区中心医院青年科研基金项目(2016-Q-01) （2016-Q-01）
