JNK磷酸化14-3-3在大鼠缺血性脑损伤中的作用  

The Effects of 14-3-3 Phosphorylation Induced by JNK on Ischemic Brain Injury in Rats

作　　者：王晓天[1] 刘晓梅[1] 汤仁仙[1] 尤红娟[1] 李小翠[1] 秦苏萍[1] 宋远见[1] 

机构地区：[1]徐州医学院病原生物学与免疫学教研室,221002

出　　处：《天津医药》2014年第7期654-656,共3页Tianjin Medical Journal

基　　金：国家自然科学基金资助项目(81371300)

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12 h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。Objective To investigate the effects of 14-3-3 phosphorylation （p-14-3-3） induced by C-Jun N-termi-nal kinase （JNK） on ischemic brain injury in rats. Methods Twenty rats were divided into 4 groups：sham operation group, ischemia-reperfusion group, SP600125 group and solvent control group. The rat model of cerebral ischemia was established. The p-14-3-3, the binding of 14-3-3 and Bax and the protein expression of Bax in cytoplasm and mitochondria in hippo-campal CA1 region were detected by immunoprecipitation （IP） and immunoblotting 12-hour after ischemia-reperfusion in four groups. Results Compared with the sham operation group, protein expression levels of p-14-3-3 in cytoplasm and Bax in mitochondria were significantly increased, the binding of 14-3-3 and Bax was significantly decreased in ischemia-re-perfusion group, solvent control group and SP600125 group. The protein expressions of p-14-3-3 and Bax were significantly lower in SP600125 group than those of ischemia-reperfusion group and solvent control group. The binding of 14-3-3 and Bax was significantly higher in SP600125 group than that of ischemia-reperfusion group and solvent control group （P ＆lt;0.05）. Conclusion 14-3-3 phosphorylation induced by JNK plays important effects on ischemic brain injury in rats.

关 键 词：14-3-3蛋白质类 JNK丝裂原活化蛋白激酶类 BCL-2相关X蛋白质 脑缺血 

分 类 号：R743.31[医药卫生—神经病学与精神病学]