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目的:观察Nur77通过线粒体转位对缺氧/复氧(H/R)诱导的心肌细胞凋亡的影响。方法:原代培养l-2天SD大鼠心肌细胞,建立H/R模型。随机分为正常对照组、H/R组、Nur77组,采用免疫荧光检测横纹肌肌动蛋白(α-actin)鉴定心肌细胞;采用TUNEL染色法及Caspase-3酶活性检测心肌细胞凋亡情况;采用Western blot检测细胞核及线粒体Nur77蛋白表达、线粒体及胞浆Omi/HtrA2蛋白表达。结果:H/R组细胞核中Nur77蛋白表达明显低于正常对照组;而在线粒体中则相反。Nur77组线粒体中的Omi/HtrA2蛋白表达明显低于正常对照组;而在胞浆中则相反。结论:在心肌细胞H/R损伤时,Nur77线粒体转位促使Omi/HtrA2蛋白从线粒体释放入胞浆,从而导致心肌细胞凋亡。
Objective: To observe the effect of Nur77 mitochondrial translocation on cardiomyocyte apoptosis induced by hypoxia / reoxygenation (H / R). Methods: primary cultured l2 days SD rat cardiomyocytes, H / R model was established. The cells were randomly divided into normal control group, H / R group and Nur77 group. Cardiomyocytes were identified by immunofluorescence staining of α-actin. Cardiomyocyte apoptosis was detected by TUNEL staining and Caspase-3 activity. Western blot was used to detect the expression of Nur77, mitochondria and cytoplasmic Omi / HtrA2 in nucleus and mitochondria. Results: The expression of Nur77 in the nucleus of H / R group was significantly lower than that in the normal control group, while in the mitochondria the opposite was found. Omi / HtrA2 protein expression in mitochondria of Nur77 group was significantly lower than that in normal control group, but opposite in cytoplasm. CONCLUSION: Mitochondrial translocation of Nur77 induces the release of Omi / HtrA2 protein from the mitochondria into the cytoplasm during cardiomyocyte H / R injury, resulting in cardiomyocyte apoptosis.