兔蛛网膜下腔出血后脑血管痉挛诱导海马组织p38 MAPK磷酸化

目的: 观察蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)模型中海马组织内p38 MAPK及其磷酸化的时相变化特点,初步探讨CVS导致缺血性脑损伤的分子机制. 方法: 用Western blot方法检测兔SAH后CVS时海马组织内p38 MAPK和磷酸化p38 MAPK (p-p38 MAPK)蛋白的表达变化.结果: p38 MAPK在SAH组各时间点的海马组织内的表达保持相对恒定,与正常对照组相比无明显变化(P > 0.05).p-p38 MAPK的表达水平在SAH组1 d时即有明显升高,4 d时达到高峰,7 d时仍维持较高的表达水平,与正常对照组相比有显著差异(P < 0.01),分别是其在正常组海马组织中表达水平的3.1,7.9和6.2倍.结论: p38 MAPK信号通路的激活可能与SAH后CVS所造成的海马神经元的损伤有密切关系.

Phosphorylation of p38-MAPK in rabbit hippocampus during cerebral vasospasm following experimental subarachnoid hemorrhage

AIM: To observe the temporal changes of p38 MAPK and its phosphorylation status in hippocampus after cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH) and to investigate the molecular mechanisms of brain injury induced by CVS. METHODS: Western blot was used to detect the changes in the expression p38 MAPK and phosphorylated p38 MAPK (p-p38 MAPK) protein in rabbit hippocampus during CVS following experimental SAH. RESULTS: The expression level of p38 MAPK protein in hippocampus kept unchanged after SAH. But the expression of p-p38 MAPK protein increased in hippocampus 1 day after injury, reached the peak at day 4 and remained relatively high level at day 7, which was significantly higher than those in the normal control group (P<0.01). CONCLUSION: The present results suggest that the activation of p38 MAPK signal pathway may closely related to the CVS-induced hippocampus injury following SAH.