| 贾敏刘静祎1 刘毅1 栗莉2 裴海峰1 刘佩林1 王瀚1 王海昌1 陶凌.Nur77 在缺氧/ 复氧诱导的心肌细胞凋亡中的作用及其机制的研究[J].现代生物医学进展英文版,2012,12(3):445-448. |
| Nur77 在缺氧/ 复氧诱导的心肌细胞凋亡中的作用及其机制的研究 |
| The Effects and Mechanism Study of Nur77 on Hypoxia／Reoxygenation-Induced Apoptosis in Rat Cardiomyocyte |
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| DOI： |
| 中文关键词: Nur77 Omi/HtrA2 心肌细胞缺氧/ 复氧损伤 凋亡 |
| 英文关键词: Nur77 Omi/HtrA2 Myocardial cell Ischemia-reperfusion injury Apoptosis |
| 基金项目: |
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| 中文摘要: |
| 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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