中国药理学通报2017，Vol.33Issue(6)：819-823,5.DOI:10.3969/j.issn.1001-1978.2017.06.015
碘化N-正丁基氟哌啶醇通过抑制线粒体凋亡通路抗H9c2心肌细胞缺氧/复氧损伤
N-n-butyl haloperidol iodide protectsH9c2 cardiac myocytes against hypoxia/reoxygenationinjury through mitochondria-dependent apoptotic pathway
摘要
Abstract
Aim To investigate the effect of N-n-butyl haloperidol iodide(F2) on mitochondria-dependent apoptotic pathway of H9c2 cardiac myocytes during hypoxia/reoxygenation(H/R) injury.Methods The H/R models of H9c2 cardiac myocytes were established.The H9c2 cardiac myocytes were randomly divided into five groups: control group(C group), hypoxia/reoxygenation group(H/R group), F2 low concentration group(L), F2 medium concentration group(M), F2 high concentration group(H).Apoptotic rate was evaluated by flow cytometry(FCM).The levels of Cyto C, Bcl-2, Bax were observed by Western blot.Caspase-3 activity was measured with colorimetry.Results Compared with H/R group, F2 low, medium and high concentrations group could significantly decrease apoptosis rate and increase the ratio of Bcl-2 to Bax proteins and inhibit the release of Cyto C into the cytosolic fraction, and decrease caspase-3 activity.Conclusion F2 can protect H9c2 cardiac myocytes against H/R-induced injury through interfering in mitochondria-dependent pathway.关键词
碘化N-正丁基氟哌啶醇/缺氧/复氧/H9c2心肌细胞/凋亡/线粒体/细胞色素CKey words
N-n-butyl haloperidol iodide/hypoxia/reoxygenation/H9c2 cardiac myocytes/apoptosis/mitochondria/cytochrome C分类
医药卫生引用本文复制引用
汪彬,黄丹梅,王远航,周巧玲,林泓,张艳美,石刚刚,郑付春..碘化N-正丁基氟哌啶醇通过抑制线粒体凋亡通路抗H9c2心肌细胞缺氧/复氧损伤[J].中国药理学通报,2017,33(6):819-823,5.基金项目
国家自然科学基金-广东省自然科学基金联合资助基金项目(No U0932005) （No U0932005）
广东省科技厅公益研究与能力建设专项资金项目(No 2014A020212290) （No 2014A020212290）
国家自然科学基金资助项目(No 81473215) （No 81473215）
