致癫痫大鼠海马中JNK/p38信号转导通路的激活及其作用  

Activation of JNK/p38 signal transduction pathway in hippocampus of epileptic rat and it′s significance

作　　者：夏杰[1] 郑铮[1] 彭玉[1] 张其梅[1] 陈阳美[2] 

机构地区：[1]三峡大学第一临床医学院神经内科,湖北宜昌443002 [2]重庆医科大学附属第二医院神经内科,400010

出　　处：《重庆医学》2011年第28期2817-2819,I0002,共4页Chongqing medicine

摘　　要：目的探讨c-Jun氨基末端激酶通路(JNK)和p38通路在癫痫持续状态(SE)大鼠海马中的活性变化规律及其意义。方法建立氯化锂-匹罗卡品癫痫持续状态模型,在不同时间点用免疫组化法检测海马结构JNK和p38磷酸化状态,并观察组织病理学改变。结果对照组P-JNK极少活化而p38在海马各结构广泛活化。SE 30 min后JNK和p38在海马神经元强烈激活,2 h时达到高峰,6 h后各区均明显减少,12 h后降至基础水平,在所有时间点,JNK和p38在齿状回的活化程度均显著高于CA1和CA3区。海马结构各区可见到许多神经元发生变性和坏死。结论 JNK和p38信号转导通路在氯化锂-匹罗卡品致痫过程中被激活,并可能在发作后参与海马神经元损伤的病理生理过程。Objective To investigate the variations of activities of the c-Jun amino terminal kinase pathway and the p38 pathway in rat hippocampus during status epilepticus（SE）and its significance.Methods The lithium-pilocarpine-induced epikpticus model was established to evaluate the phosphorylation forms of JNK and p38 by immunohistochemistry and observe histopathology changes at different times after piocarpine injection.Results The JNK was scarcely activated and phospho-p38 immunoreactivity was observed widely in saline-treated rats hippocampal formation.In pilocarpine-treated rats,the hippocampal neurons showed a strong immunoreactivity of phospho-JNK and phospho-p38 at 30min which peaked at 2h after pilocarpine injection,while decreased markedly at 6h and returned to basal level at 12h.At all time points,activation states of JNK and p38 in the dentate gyrus were significantly higher than the CA1 and CA3 areas.Many injured neurons were found in hippocampus of SE rats.Conclusion JNK and p38 signal transduction pathway could be activated in lithium-pilocarpine-induced epilepticus model,and may participate in the pathophysiology of hippocampal neurons damage.

关 键 词：P38丝裂原活化蛋白激酶类 癫痫 海马 C-JUN氨基末端激酶 

分 类 号：R742.1[医药卫生—神经病学与精神病学]