有氧运动通过上调Dhcr24改善H2O2诱导的心肌细胞凋亡

目的 研究Dhcr24在有氧运动改善心肌梗死(myocardial infarction,MI)后心肌细胞功能中的潜在作用及分子机制。方法 通过H2O2建立心肌细胞(H9C2)凋亡模型,并通过AMPK激动剂AICAR来模拟心肌细胞的运动效果。通过流式细胞术和TUNEL检测心肌细胞凋亡水平；通过Western blot检测心肌细胞中凋亡相关蛋白Bcl-2、Bax和Dhcr24的表达水平；通过RT-qPCR检测细胞中Dhcr24 mRNA的水平。结果 与对照组相比,H2O2诱导的心肌细胞凋亡率增加、TUNEL阳性粒子数升高、抗凋亡蛋白Bcl-2水平降低、促凋亡蛋白Bax水平升高、Dhcr24水平降低。与H2O2诱导的心肌细胞相比,AMPK激活剂AICAR处理后,心肌细胞凋亡率、TUNEL阳性粒子数降低、Dhcr24水平升高。在H2O2和AICAR共同处理的心肌细胞中敲低Dhcr24,降低的细胞凋亡率、TUNEL阳性粒子数得到逆转。结论 有氧运动对H2O2诱导的心肌细胞凋亡具有明显保护作用,可能与其上调Dhcr24表达有关。

Aerobic Exercise Improves H2O2-Induced Apoptosis in Cardiomyocyte Cells through upregulating Dhcr24

Objective To study the potential role and molecular mechanism of Dhcr24 in improving cardiomyocyte function after myocardial infarction (MI) by aerobic exercise. Methods The apoptosis model of cardiomyocytes (H9C2) was established by H2O2, and the exercise effect of cardiomyocytes was simulated by AMPK agonist (AICAR). The apoptosis level of cardiomyocytes was detected by flow cytometry and TUNEL; the expression levels of apoptosis-related proteins (Bcl-2 and Bax) and Dhcr24 were detected by Western blot; the level of Dhcr24 mRNA was detected by RT-qPCR. Results Compared with the control group, H2O2 induced increased cell apoptosis, the number of TUNEL-positive particles and pro-apoptotic protein Bax level, and decreased the level of anti-apoptotic protein Bcl-2 and Dhcr24. Compared with cardiomyocytes induced by H2O2, AICAR treatment decreased the apoptotic rate, the number of TUNEL-positive particles, and increased the level of Dhcr24. In cardiomyocytes treated with H2O2 and AICAR, knockdown of Dhcr24 reversed the decreased apoptosis rate and the number of TUNEL-positive particles. Conclusion Aerobic exercise can play a significant protective effect on cardiomyocyte apoptosis induced by H2O2, which may be related to the upregulation of Dhcr24.