JNK信号通路介导大鼠局灶性脑缺血再灌后海马神经元凋亡  

APOPTOSIS IN HIPPOCAMPUS AFTER FOCAL CEREBRAL ISCHEMIA REPERFUSION THROUGH JNK SIGNALING PATHWAY IN RATS MODELS

作　　者：田艳霞[1] 刘江[2] 高俊玲[1] 李冉[1] 刘丽娜[1] 

机构地区：[1]华北煤炭医学院组织胚胎学教研室,唐山063000 [2]华北煤炭医学院解剖教研室

出　　处：《现代预防医学》2008年第21期4267-4269,共3页Modern Preventive Medicine

基　　金：河北省科技领军人才基金(博士基金)(06547008D-7)

摘　　要：[目的]研究局灶性脑缺血再灌(I/R)后c-Jun氨基端激酶(JNK)蛋白表达及其依赖的caspase途径激活情况,探讨此通路在海马神经元凋亡中可能的作用及机制。[方法]建立大鼠可逆性大脑中动脉栓塞(MCAO)模型,采用免疫印迹法检测不同实验组中海马区p-c-jun及凋亡Caspase-3表达,TUNEL法原位检测CA1区凋亡锥体细胞。[结果]与假手术组比较,模型组p-c-jun蛋白平均灰度值显著增强,以3h、6h、12h差异有统计学意义(P﹤0.05)。模型组Caspase-3于再灌注后6h开始表达(P﹤0.05),12h其条带密度达高峰(P﹤0.05)。I/R3h至24h海马区p-c-jun表达与caspase-3呈正相关(r=0.696,P﹤0.01);caspase-3与TUNEL呈正相关(r=0.310,P﹤0.01)。[结论]大鼠I/R后JNK部分激活了Caspase依赖的促凋亡通路。[Objective] To investigate the expression and mechanism of c-Jun N.terminal .protein kinase （JNK） protein-dependent activation of caspase signaling pathway in the nerve cell＇ s apoptosis in hippocampus in rats after focal cerebral ischemia reperfusion （I/R）. [ Methods] Replicated the MCAO model of rats. The tissues of hippocampus of rats were sampled, the expression of JNK and easpase-3 protein were determined by Western blotting. The apoptosis of pyramidal neurons Was detected by TUNEL method. [ Results] As comparing with the sham group, the p-c-jun level in the I/R group was significanfly enhanced; difference was significant between 3 h, 6 h, 12 h （P〈 0.05）. Caspase-3 appeared at 6h after reperfusion （P 〈 0.05） i and it＇s peaked at 12 h （P 〈 0.05）. The quantification of p-c-Jun expression in hippocampus was positively correlated with the expressions of Caspase-3 （r = 0.696, P 〈 0.01 ） and the expression of p-c＇Jun was positively correlated with the expressions of TUNEL positive cells after I/R （r = 0.310, P 〈 0.01 ）. [Conclusion] JNK-dependent activation of caspase signaling pathway partly activates the signal transudation of the apoptosis after I/R.

关 键 词：大脑中动脉阻塞 局灶性脑缺血再灌注 c—Jun氨基端激酶 半胱氨酸天冬氨酸特异性蛋白酶 凋亡 

分 类 号：R741[医药卫生—神经病学与精神病学]