山东医药2011，Vol.51Issue(1)：24-26,3.
JNK通路在内质网应激预处理诱导脑缺血耐受中的作用
Effect of the JNK pathway in the brain ischemic tolerance induced by endoplasmic reticulum stress preconditioning
摘要
Abstract
Objective To investigate the effect and the mechanism of the JNK pathway in hippocampal CA1 area ischemic tolerance induced by endoplasmic reticulum stress preconditioning. Methods 216 SD rats were randomly divided into sham (SH) group, ischemia/reperfusion (I/R) group, endoplasmic retieulum stress preeonditioning ( IP ) group, IP + I/R group( IP + I/R), Curcumin + I/R(CU) group, Curcumin + IP + I/R(CP) group, Anisomycin + I/R group( AN),Anisomycin + IP + I/R (AP)group and solvent control + I/R(VE) group. In hippocampal CA1 area, using TUNEL to test apoptosis, using immunohistochemistry and Westem-Blot to find the difference of GRP78, p-JNK and c-jun. Results SH had a little GRP78 protein. Compared with SH, I/R, CU, AN and VE increased (P＜0.05); IP, IP + IR, CP, AP increased significantly ( P ＜ 0.01 ). Compared with the IP, IP + IR, CP, AP increased ( all P ＜ 0.05). Compared with I/ R, IP + I/R, CU and CP rednced the number of apoptosis cells and p-JNK and c-Jun ( all P ＜ 0.01 ). The effect of that was CP＞IP＞CU; AN increased the number of apoptosis cells and enhanced p-JNK and c-Jun(P ＜0.01); AP offsetted the protection of IP partially. Conclusions The activation of JNK pathway is involved in ischemic neuronal apoptosis in hippocampal CA1 area. Endoplasmic reticulum stress preconditioning may inhibit JNK phosphorylated and reduce c-Jun to protect hippocampal CA1 area neurons. To inhibit the activation of JNK pathway may play a similar protective effect of endoplasmic reticulum stress.关键词
内质网应激/缺血预处理/自身耐受性/GRP78/JNKKey words
endoplasmic reticulum stress/ ischemic preconditioning/ self tolerance/ GRP778/ JNK分类
医药卫生引用本文复制引用
刘丽华,闵鹤鸣,闵连秋..JNK通路在内质网应激预处理诱导脑缺血耐受中的作用[J].山东医药,2011,51(1):24-26,3.基金项目
辽宁省自然科学基金项目(20092192). （20092192）
