兔痉挛脑血管中JNK的表达及其抑制剂的影响

目的 观察兔脑血管痉挛（CVS）后基底动脉p-jnk的表达及其抑制剂SP600125对其表达的影响，以探讨蛛网膜下腔出血（SAH）后CVS细胞信号转导通路机制。方法 ①采用二次枕大池注血建立家兔CVS模型。②采用HE染色、免疫组织化学技术动态观察兔基底动脉血管壁组织病理改变、p-jnk的表达及使用SP600125干预后对上述表达的影响。结果 ①SAH组基底动脉管腔狭窄、炎症细胞浸润等，以SAH后7d时为最重，10d时逐渐缓解；SAH＋SP600125组与同时段的SAH组比较血管变化明显减轻。②SAH组p-jnk在SAH后7d时表达最为明显，10d表达稍减少，但仍明显高于正常组（P〈0．01）；SAH＋SP600125组与同时段的SAH组比较p-jnk表达明显减少（P〈0．05）。结论 ①原癌基因c-jun氨基末端激酶（JNK）信号转导通路调节免疫炎性反应，是参与形成CVS机制之一。②JNK抑制剂SP600125可以调控血管壁的炎症反应，有效缓解CVS。

Expression of JNK in Spasmodic Cerebral Vessels and Effect of JNK inhibitor,SP600125 on Its Expression in Rabbits

Objective To observe the expression of p-jnk in the basilar arteries after cerebral vasospasm（CVS） and the effect of its inhibitor, SP600125 on CVS and p-jnk expression in rabbits in order to explore signal pathway nieehanism in CVS after subai＇aehnoid hemorrhage（SAH）. Methods ①The model of CVS after SAH was established in the rabbits. ②The pathological changes and the expression of p-jnk in the basilar arteries of the rabbits were determined respectively by HE staining and immunohistochemieal techniques. The effects of sp600125 on CVS and p-jnk expression were observed. Results ①The＇lumens of the basilar arteries became narrow and their vascular walls were infiltrated into by inflammatory cells in SAH group, where the most significant changes in the basilar arteries were found 7 days, and the changes were relieved gradually 10 days after SAH. The change in the basilar arteries of SAH＋SP600125 group was significantly alleviated compared to that of SAH group. ②There was the most significant expression of p-jnk 7 days after SAH and it was decreased 10 days after SAH, but it was still significantly higher than that in normal group （P〈0.01）. The expression of p-jnk in SAH＋SP600125 group was significantly lower than that in SAH group 4, 7 and 10 days after SAH （P〈0.05）. Conclusions That e-jun N-terminal kinase （JNK） signal pathway regulates immune and inflammatory reactions is one of mechanism producing CVS. ②JNK inhibitor, SP600125 may regulate inflammatory reaction of vessel walls and effectively alleviate CVS after SAH in the rabbits.