JNK磷酸化Bad在脑缺血神经元凋亡中的作用  

Effects of Bad phosphorylation induced by JNK on cerebral ischemic neuronal apoptosis

作　　者：王晓天[1] 刘晓梅[1] 尤红娟[1] 李小翠[1] 秦苏萍[1] 汤仁仙[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,江苏徐州221002

出　　处：《中国现代医生》2014年第31期1-3,7,共4页China Modern Doctor

基　　金：国家自然科学基金资助项目(81371300)

摘　　要：目的探讨JNK磷酸化Bad在大鼠缺血性神经元凋亡中的作用。方法 20只大鼠均分为4组:假手术组、缺血复灌组、溶剂对照组和SP600125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大鼠脑缺血复灌1 d海马CA1区神经元Bad与14-3-3及Bad与Bcl-Xl的结合、Bad丝氨酸128位磷酸化[p-Bad(S128)]水平、Caspase-3蛋白表达情况。结果与缺血复灌组相比,SP600125组海马CA1区神经元Bad与14-3-3的结合明显增高,Bad与Bcl-Xl的结合、p-Bad(S128)、Caspase-3表达显著减少(均P<0.05)。结论 JNK介导的Bad(S128)磷酸化在大鼠缺血性脑损伤中发挥了重要作用。Objective Investigate the effects of Bad phosphorylation induced by JNK on cerebral ischemic neuronal apoptosis in rats. Methods Twenty rats were divided into 4 groups averagely： sham operation group, ischemia-reperfusion group, sol- vent control group and SP600125 group. Making rat model of cerebral ischemia, the binding of Bad and 14-3-3 ,the binding of Bad and Bcl-X1, Bad phosphorylation at serine 128（p-Bad（S128）） and Caspase-3 protein expression in hippocampal CA1 region were detected by immunoprecipitation （IP） and immunoblotting （IB） ld after isehemia-reperfusion. Results Compared with the isehemia-reperfusion group, the binding of Bad and 14-3-3 was increased, the binding of Bad and Bcl-X1, p-Bad （S128） and Caspase-3 protein expression in hippocampal CA1 region were decreased in SP600125 group （All P〈0.05）. Conclu- sion Bad phosphorylation at serine 128 induced by JNK playe important effects on cerebral ischemic neuronal apoptosis in rats.

关 键 词：BAD JNK丝裂原活化蛋白激酶类 凋亡 脑缺血 

分 类 号：R743.31[医药卫生—神经病学与精神病学]