天津医药

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JNK磷酸化14-3-3在大鼠缺血性脑损伤中的作用

王晓天,刘晓梅,汤仁仙,尤红娟,李小翠,秦苏萍,宋远见   

  1. 徐州医学院
  • 收稿日期:2014-02-19 修回日期:2014-04-08 出版日期:2014-07-15 发布日期:2014-07-15
  • 通讯作者: 王晓天

The Effects of14-3-3Phosphorylation Induced by JNK on Ischemic Brain Injury in Rats

  • Received:2014-02-19 Revised:2014-04-08 Published:2014-07-15 Online:2014-07-15

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摘要：

【摘要】目的 探讨c-Jun氨基末端激酶（JNK）磷酸化14-3-3在大鼠缺血性脑损伤中的作用。方法 20只大鼠均分为4组：假手术组、缺血复灌组、SP600125组和溶剂对照组。制作大鼠全脑缺血模型，应用免疫沉淀和免疫印迹法检测4组大鼠脑缺血复灌12h海马CA1区神经元14-3-3磷酸化（p-14-3-3）、14-3-3与Bax结合、Bax在胞浆和线粒体的蛋白表达情况。结果与假手术组相比，缺血复灌组、溶剂对照组及SP600125组胞浆中的p-14-3-3蛋白、线粒体中的Bax蛋白均增高，14-3-3与Bax的结合降低，SP600125组的胞浆p-14-3-3蛋白、线粒体Bax蛋白低于缺血复灌组和溶剂对照组，14-3-3与Bax的结合高于缺血复灌组和溶剂对照组（均P<0.05）。结论JNK磷酸化14-3- 3在大鼠缺血性脑损伤中发挥了重要作用。

关键词: 14-3-3磷酸化, JNK, Bax, 脑缺血

Abstract: Objective: Investigate the important effects of 14-3-3 phosphorylation induced by JNK on ischemic brain injury in rats. Methods: Reproduced the four-vessel occlusion model of cerebral ischemia in rats. 14-3-3 phosphorylation, the binding of 14-3-3 and Bad, protein expression of Bax in cytoplasm and mitochondria in hippocampal CA1 region were detected by immunoprecipitation (IP) and immunoblotting (IB) 12 hour after ischemia reperfusion. Results: Compared with the sham operation group, SP600125, an inhibitor of JNK, inhibited 14-3-3 phosphorylation, promoted the binding of 14-3-3 and Bad, lessened the expression of Bax in mitochondria in hippocampal CA1 region. Conclusion: 14-3-3 phosphorylation induced by JNK played important effects on ischemic brain injury in rats, which provided a new idea for clinical control of human ischemic stroke.

Key words: 14-3-3 phosphorylation, JNK, Bax, Cerebral ischemia