曲美他嗪对缺氧诱导原代大鼠心肌细胞凋亡的影响

发布时间：2019-01-26 07:34

【摘要】：目的研究曲美他嗪对缺氧诱导的心肌细胞凋亡及线粒体能量代谢改变的影响。方法采用胰酶和胶原酶联合消化的方法,提取大鼠原代心肌细胞,三气培养箱模拟缺氧损伤。MTT和Hoechst染色检测细胞活性和凋亡,TMRE染色检测线粒体膜电位,Oxygraph-2k细胞呼吸测量仪检测态3、态4呼吸和呼吸控制率,Western blot检测Caspase-3、细胞色素C以及线粒体呼吸链复合酶体Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ蛋白表达水平的变化。结果缺氧能够诱导心肌细胞凋亡、引起线粒体膜电位下降和促进细胞色素C的释放。此外,缺氧能够显著下调态3呼吸和上调态4呼吸,引起呼吸控制率的下降,同时缺氧能够不同程度地下调线粒体呼吸链复合酶体Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ的蛋白表达水平。曲美他嗪能够显著降低缺氧诱导的心肌细胞凋亡、稳定线粒体膜电位和减少细胞色素C释放。此外,曲美他嗪还能减轻缺氧对线粒体呼吸链复合酶体的损伤,维持线粒体有氧呼吸。结论曲美他嗪具有抵抗缺氧致心肌细胞凋亡的作用,可能与其稳定线粒体膜和呼吸链复合酶体有关,继而减少细胞色素C的释放和维持线粒体有氧呼吸。
[Abstract]:Aim to study the effects of trimetazidine on hypoxia-induced myocardial apoptosis and mitochondrial energy metabolism. Methods Primary rat cardiomyocytes were extracted by combined digestion of trypsin and collagenase, anoxic injury was simulated in three air incubators, cell activity and apoptosis were detected by MTT and Hoechst staining, mitochondrial membrane potential was detected by TMRE staining. The expression levels of Caspase-3, cytochrome C and mitochondrial respiratory chain complex enzymes 鈪，

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