蛛网膜下腔出血后大鼠基底动脉p38MAPK信号传导途径研究

p38MAPK signal pathway in basilar artery after subarachnoid hemorrhage

目的探讨蛛网膜下腔出血(SAH)后大鼠基底动脉中p38丝裂原活化蛋白激酶(p38MAPK)信号传导通路的活化情况以及与脑血管痉挛(CVS)的关系。方法通过枕大池二次注血方法制作大鼠SAH模型,以免疫组化方法和逆转录酶-多聚酶链反应分析,分别从蛋白、基因水平分析SAH后基底动脉中p38MAPK信号传导通路的活化情况。结果 SAH后大鼠基底动脉逐渐出现痉挛。基底动脉磷酸化p38MAPK表达逐渐增加,3 d时达高峰并持续至第5 d,14 d时恢复正常。p38MAPK基因表达在注血后1 d明显增加,逐渐增加,于5 d时达高峰,14 d仍维持较高水平。结论SAH后大鼠基底动脉中p38MAPK信号传导通路激活,可能诱导CVS的发生。

Objective To investigate the activity and expression of the p38 mitogen activated protein kinase（p38MAPK） pathway and the possible role of p38MAPK in the pathogenesis of cerebral vasospasm in a rat double-hemorrhage model.Methods Subarachnoid hemorrhage（SAH） model was established according to the double-hemorrhage method.Immunohistochemical staining was used to assess the expression of p-p38MAPK,and the gene of p38MAPK after SAH was examined by reverse transcription polymerase chain reaction（RT-PCR）.Results Vasospasm presented in the basilar artery gradually after SAH.The expression of p-p38MAPK was increased gradually at 1 d after SAH,reached its peak at 3 d and lasted till 5 d,and returned to baseline levels at 14 d.p38MAPK mRNA expressions started to increase at 1 d and reached its peak at 5 d after SAH,and remained the high level at 14 d.Conclusion The p38MAPK pathway is activated after SAH,and may lead to the development of cerebral vasospasm after SAH.