[1]蔡少艾,陈景福,陈美姬,等.血管紧张素-(1-7)通过抑制ClC-3通道减轻高糖引起的心肌细胞损伤[J].南方医科大学学报,2017,(07):895.
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血管紧张素-(1-7)通过抑制ClC-3通道减轻高糖引起的心肌细胞损伤()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2017年07期
页码:
895
栏目:
出版日期:
2017-07-20

文章信息/Info

Title:
Angiotensin-(1-7) protects cardiac myocytes against high glucose-induced injury by inhibiting ClC-3 chloride channels
作者:
蔡少艾陈景福陈美姬林健聪冯鉴强林凯智喜梅张伟杰吴文
关键词:
血管紧张素-(1-7)ClC-3通道高糖心肌细胞损伤
Keywords:
angiotensin-(1-7) ClC-3 chloride channels high glucose cardiac cells cell injury
摘要:
目的探讨血管紧张素-(1-7)[Ang-(1-7)]能否通过调控ClC-3 通道保护心肌细胞对抗高糖引起的损伤。方法应用 35 mmol/L葡萄糖处理H9c2心肌细胞24 h建立损伤模型。Ang-(1-7)或氯通道抑制剂与心肌细胞共处理24 h观察对高糖诱发 的心肌细胞损伤的影响。应用细胞计数试剂盒8检测细胞存活率;Hoechst33258染色荧光显微镜照相术检测凋亡细胞的形态 学改变;双氯荧光素染色荧光显微镜照相术测定细胞内活性氧水平;超氧化物歧化酶试剂盒测定活性;罗丹明123染色荧光显 微镜照相术检测线粒体膜电位;Western blot法测定心肌细胞ClC-3通道蛋白的表达水平。结果35 mmol/L葡萄糖处理H9c2 心肌细胞24 h明显地增加ClC-3通道蛋白的表达水平(P<0.01);1 μmol/LAng-(1-7)与葡萄糖共处理心肌细胞24 h显著地抑制 葡萄糖对ClC-3通道蛋白表达的上调作用(P<0.01);1 μmol/LAng-(1-7)或100 μmol/L氯通道抑制剂氯通道抑制剂与葡萄糖共 处理心肌细胞24 h减轻葡萄糖引起的损伤作用,表现为增加细胞存活率和超氧化物歧化酶活性,减小细胞凋亡数量,胞内活性 氧水平及线粒体膜电位丢失(P<0.01)。结论ClC-3通道参与葡萄糖引起的心肌细胞损伤;Ang-(1-7)通过抑制ClC-3通道保护 心肌细胞对抗葡萄糖引起的损伤。
Abstract:
Objective To explore whether angiotensin-(1-7) [Ang-(1-7)] protects cardiac myocytes against high glucose (HG)-induced injury by inhibiting ClC-3 chloride channels. Method H9c2 cardiac cells were exposed to 35 mmol/L glucose for 24 h to establish a cell injury model. The cells were treated with Ang-(1-7) or the inhibitor of chloride channel (NPPB) in the presence of HG for 24 h to observe the changes in HG-induced cell injury. Cell counter kit 8 (CCK-8) assay was used to test the cell viability, and the morphological changes of the apoptotic cells were detected using Hoechst 33258 staining and fluorescent microscopy. The intracellular level of reactive oxygen species (ROS) was examined by DCFH-DA staining, SOD activity in the culture medium was measured using commercial kits, and the mitochondrial membrane potential (MMP) of the cells was tested with rodamine 123 staining. The expression level of cardiac ClC-3 chloride channels was detected with Western blotting. Results Exposure of H9c2 cardiac cells to 35 mmol/L glucose for 24 h markedly enhanced the expressions of cardiac ClC-3 channel protein (P<0.01). Co-treatment of the cells with 1 μmol/L Ang-(1-7) and HG for 24 h significantly attenuated HGinduced upregulation of ClC-3 channel protein expression (P<0.01). Co-treatment of the cells exposed to HG with 1 μmol/L Ang-(1-7) or 100 μmol/L NPPB for 24 h obviously ameliorated HG-induced injuries as shown by increased cell viability, enhanced SOD activity, decreased number of apoptotic cells, and reduced intracellular ROS generation and loss of MMP (P< 0.01). Conclusion ClC-3 channels are involved in HG-induced injury in cardiac cells. Ang-(1-7) protects cardiac cells against HG-induced injury by inhibiting ClC-3 channels.

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更新日期/Last Update: 1900-01-01