翟春丽.视神经萎缩相关蛋白A1在缺氧心肌细胞凋亡中的抑制作用[J].内科急危重症杂志,2019,25(6):496-499
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| DOI：10.11768/nkjwzzzz20190616 |
| 中文关键词: 心肌细胞 视神经萎缩相关蛋白A1 线粒体融合 活性氧 凋亡 |
| 英文关键词: |
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| 中文摘要: |
| 目的：探讨视神经萎缩相关蛋白A1（OPA1）在缺氧心肌细胞凋亡中的保护作用。方法：利用小干扰RNA（siRNA）在体外下调OPA1表达后，采用流式检测下调OPA1对缺氧心肌细胞凋亡的影响；用Western blot检测下调OPA1对缺氧心肌细胞线粒体细胞色素C释放及含半胱氨酸的天冬氨酸蛋白水解酶Caspase-3与Caspase-9活性的影响；用流式分析下调OPA1对缺氧心肌细胞活性氧(ROS)产生的影响。结果：下调OPA1可明显加重缺氧诱导的心肌细胞凋亡，诱导线粒体细胞色素C释放并激活Caspase-3与Caspase-9活性，诱导心肌细胞中ROS产生。结论：OPA1分子具有抑制缺氧心肌细胞凋亡的作用，其机制可能是OPA1介导的线粒体融合抑制了线粒体中细胞色素C的释放与ROS的生成。 |
| 英文摘要: |
| Objective:To explore the protective role of optic atrophy type 1(OPA1) in apoptosis of cardiomyocytes during hypoxia. Methods: Cell apoptosis was evaluated by flow cytometry after knocking down OPA1 with siRNA in cardiomyocytes during hypoxia; Cytochrome C release and activities of caspase-3 and caspase-9 were evaluated by Western blot analysis after knocking down OPA1 with siRNA in cardiomyocytes during hypoxia; Reactive oxygen species (ROS) production was determined by flow cytometry after knocking down OPA1 with siRNA in cardiomyocytes during hypoxia. Results: Knockdown of OPA1 significantly aggravated hypoxia-induced apoptosis of cardiomyocytes; significantly increased hypoxia-induced cytochrome C release from mitochondria, and activities of caspase-3 and caspase-9; significantly increased hypoxia-induced ROS production. Conclusion: OPA1-regulated mitochondrial fusion may play an important protective role in cardiomyocytes from hypoxia-induced cell apoptosis mainly through inhibition of cytochrome C release and ROS production. |
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