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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。
Objective: To study the role of JNK signaling pathway in inducing cerebral ischemic tolerance and to observe the regulation effect of Shuxuetongmai Capsule preconditioning. Methods: Rats were subjected to ischemic preconditioning for 3 min to induce cerebral ischemic tolerance in rats. After 24 h, a rat model of cerebral ischemia-reperfusion was established (ischemic preconditioning group). The expression of JNK , P-JNK in rat model of cerebral ischemic preconditioning, and compared with sham operation group, cerebral ischemia-reperfusion group and Shuxuetong Capsule group. Tunel method was used to detect neuronal apoptosis The number of death, observed JNK, P-JNK expression levels and neuronal apoptosis correlation. Results: Compared with the model group, the expression of P-JNK in ischemic preconditioning group and Shuxuetongmai capsule group were significantly decreased (P <0.05), and the number of neuronal apoptosis was significantly decreased (P <0.05). Conclusion: Cerebral ischemic preconditioning can reduce neuronal apoptosis and improve neurological function after cerebral ischemia and reperfusion, and its mechanism is related to the inhibition of JNK signaling pathway. Shuxuetongmai capsule preconditioning may play a role in cerebral protection by inhibiting this pathway effect.