摘要
目的 研究JAK2/STAT3信号通路在脑缺血再灌注损伤后的表达情况,并观察Rho激酶抑制剂Y-27632对其调控作用.方法 建立大鼠脑缺血再灌注模型,应用免疫组织化学染色法检测P-JAK2、P-STAT3在梗死区的表达水平,Tunel法检测神经细胞凋亡数量,观察P-JAK2、p-STAT3表达水平与神经元凋亡的相关性.结果 脑缺血再灌注后P-JAK2以及P-STAT3表达均上调,给予P-JAK2抑制剂以及Y-27632后,P-JAK2、P-STAT3的表达均受到抑制,同时减少了神经元凋亡数量,与模型组比较,差异均有统计学意义（P＜0.05）.结论 脑缺血再灌注后JAK2/STAT3信号通路激活,Y-27632可能通过抑制该通路的激活起到减少神经元凋亡,减轻神经功能缺损等脑保护作用.
Objective To observe the expression of the JAK2/STAT3 signal pathway in the cerebral ischemia- reperfusion injury in rats, and the regulation of Rho kinase inhibitor Y- 27632. Methods Cerebral ischemia reperfusion model was established. The expression of P--JAK2 and P-- STAT3 in the infarct area were detected with immunohistochemistry and the apoptosis were observed with Tunel. We also investigated the relationship between the activation of JAK2/STAT3 and apoptosis. Results There was an improvement in the expression of P--JAK2 and P--STAT3 after cerebral ischemia--reperfusion. The inhibitor of P--JAK2 and Y--27632 blocked post--iscbemic JAK2 and STAT3 phospborylation while the amount of apoptosis declining. Comparing to the model group, were significantly（P〈0.05）. Conclusions JAK2/STAT3 signal pathway were activated after cerebral iscbemia-- reperfusion, Y--27632 can decline the neuronal apoptosis and improve the neural function through sup- pressing the signal pathway.
出处
《神经疾病与精神卫生》
2013年第6期603-606,共4页
Journal of Neuroscience and Mental Health
基金
广西中医药大学附属瑞康医院科研课题（RPK201014）
