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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。

英文摘要:

Objective: To investigate mitochondrial translocation of Nur77 on hypoxia/reoxygenation-induced apoptosis in rat cardiomyocyte. Methods: A model of cultured cardiomyocytes from neonatal rats of hypoxia/reoxygenation-induced apoptosis was established, and randomly devided into three groups: control group, H/R group and Nur77 group. Immunohistochemistry of α-actin with confocal microscopy was used to detect the identification in cardiomyocytes. TUNEL staining was used to detect morphological changes of apoptotic cells. Colorimetry was used to detect caspase-3 activity was used to detect apoptotic rates. Expression of Nur77 protein of nucleus and mitochondria was measured by Western blot. Expression of Omi/HtrA2 protein of mitochondria and cytosolic was measured by Western blot. Results：Compared with that in control and H/R groups, the expression of Nur77 protein of nucleus was markedly attenuated in H/R groups, but it was opposite in mitochondria. Compared with that in control and Nur77groups, the expression of Omi/HtrA2 protein of mitochondria was markedly attenuated in Nur77 groups, but it was opposite in cytosolic. Conclusion： Mitochondrial translocation of Nur77 mediates Omi/HtrA2 to release on hypoxia/reoxygenation-induced apoptosis.

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