Grp78和caspase-12在缺氧心肌细胞中的表达

Expression of glucose-regulated protein 78 and caspase-12 in hypoxic rat cardiomyocytes

  • 摘要: 目的 利用体外培养的心肌细胞缺氧模型,观察不同缺氧时间点Grp78和caspase-12在心肌细胞中的表达变化。方法 将原代培养的大鼠心肌细胞,随机分为正常对照组,缺氧0.25h、0.5h、1h、1.5h、2h、4h、8h、12h、16h、24h组,通过TUNEL法检测缺氧心肌细胞凋亡,应用Westernblot法检测不同缺氧时间点Grp78和caspase-12在心肌细胞中的表达。结果 与对照组相比,缺氧组细胞凋亡指数随缺氧时间延长逐渐升高;Grp78蛋白于缺氧0.25h开始表达,缺氧1h达到峰值;procaspase-12于缺氧0.5h表达开始增高,2h达到峰值;caspase-12于缺氧1h表达上升,4h达到峰值。结论 缺氧激活了内质网应激反应,可引起心肌细胞凋亡。

     

    Abstract: Objective To observe the expression of glucose-regulated protein 78 (Grp78) and caspase-12 in hypoxic rat cardiomyocytes. Methods Neonatal rat cardiomyocytes were randomly divided into control group and hypoxia 0.25h,0.5h,1h,1.5h,2h,4h,8h,12h,16h,24h groups.Apoptosis was assayed by TUNEL.Expression of Grp78 and caspase-12 was detected by Western blot at different time points. Results Compared with the control group,the apoptotic index increased with hypoxia time,the expression of Grp78 increased at 0.25h after hypoxia and reached its peak at 1h.The expression of procaspase-12 protein in the hypoxic group increased at 0.5h and reached its peak at 2h after hypoxia.The expression of caspase-12 increased at 1h and reached its peak at 4h after hypoxia compared with the control group. Conclusion Hypoxia can induce ER stress response,and endoplasmic reticulum stress is involved in apoptosis of cardiomyocytes after hypoxia.

     

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