JNK信号通路在脑缺血耐受诱导中的作用及疏血通脉胶囊预处理对其调控作用研究

Function of JNK Signaling Pathway in Induction of Brain Ischemic Tolerance and Regulation of Shu-Xue Tong-Mai Capsule Pretreatment

目的:研究JNK信号通路在脑缺血耐受诱导中的作用,并观察疏血通脉胶囊预处理对其调控作用。方法:对大鼠进行3 min脑缺血预处理,诱导大鼠产生脑缺血耐受,24 h后建立大鼠脑缺血再灌注模型(缺血预处理组),应用免疫印迹法观察JNK、P-JNK在大鼠脑缺血预处理模型中的表达情况,并与假手术组、脑缺血再灌注组、疏血通脉胶囊组的表达水平进行比较,应用Tunel法检测神经元凋亡数量,观察JNK、P-JNK的表达水平与神经元凋亡的相关性。结果:与模型组相比,缺血预处理组及疏血通脉胶囊组P-JNK表达水平均明显下降(P<0.05),同时神经元凋亡数量明显减少(P<0.05)。结论:脑缺血预处理能够减少脑缺血再灌注后神经元的凋亡,改善神经功能,其机制与JNK信号通路抑制有关,疏血通脉胶囊预处理可能通过抑制该通路起到脑保护作用。

This study was aimed to explore the function of c-Jun N-terminal kinase （JNK） signaling pathway in the induction of brain ischemic tolerance, and observe the function of Shu-Xue Tong-Mai （SXTM） capsule pretreatment. Ischemic preconditioning was performed for 3 min on rats to induce cerebral ischemic tolerance. Rat model of cere-bral ischemia reperfusion （the ischemia pretreatment group, I/R group） was established 24 h later. Western blot was used to detect the protein expression of JNK and phosphorylation of c-Jun N-terminal kinase （P-JNK）, comparing to the expression with the sham operation group, I/R group and SXTM capsule group. Tunel method was applied to de-tect the apoptosis of neurons. Relationship between expression of JNK, P-JNK and apoptosis of neurons was also studied. The results showed that compared with the model group, expressions of P-JNK in ischemia preconditioning group and SXTM group were declined significantly （P 〈 0.05）; and the apoptosis of neurons quantity was also de-clined （P〈 0.05）. It was concluded that ischemia preconditioning can decrease the apoptosis of neurons in cerebral ischemia reperfusion, and improve neurologic function. Its mechanism related to the inhibition of JNK signaling path-way. SXTM capsule pretreatment can protect the cerebral by inhibiting the JNK signaling pathway.