中文摘要：

目的探讨p38MAPK特异性抑制剂SB203580在迟发性脑血管痉挛（CVS）形成中的可能作用机制。方法 24只兔均分为四组：空白对照组枕大池注入生理盐水;其余3组采用枕大池二次注血法建立兔蛛网膜下腔出血（SAH）模型。SAH组为模型对照;二甲基亚砜（DMSO）组枕大池注入载体DMSO;SB组枕大池注入SB203580。采用免疫组化和RT-PCR法检测血管壁IL-6、细胞间黏附分子1（ICAM-1）蛋白和mRNA表达。结果 SAH组和DMSO组基底动脉壁IL-6、ICAM-1蛋白和mRNA表达均较对照组明显上调（P〈0.05）;SB组在基底动脉痉挛改善的同时,基底动脉壁IL-6、ICAM-1蛋白和mRNA表达较SAH组和DMSO组明显下调（P〈0.05）。结论 SB203580明显抑制SAH后脑血管壁IL-6、ICAM-1的表达,提示p38MAPK可能通过SAH后脑血管壁炎症反应参与了SAH后CVS形成的病理过程。

英文摘要：

Objective To investigate the possible mechanism of p38 mitogen-activated protein kinase（p38 MAPK） in the development of cerebral vasospasm （CVS） in experimental subarachnoid hemorrhage（SAH） of rabbits. Methods Twenty-four rabbits were egually divided into blank control group（C） and three SAH model groups of SAH （model control）, DMSO（cisterna magna-inj ected with vehical dimethyl sulfoxide）,and SB（cisterna magna-injected with SB203580）. The expressions of IL-6 and intercellular adhesion molecule （ICAM）-1 in cerebral vascular wall were detected with immunohistochemical technique and RT-PCR. Results The protein and mRNA expressions of IL-6 and ICAM-1 in arterial wall were higher in groups of SAH and DMSO than those in group C （P〈0. 05）, which were significantly downregulated in group SB （P〈0. 05 ）. Conclusion The expressions of IL-6 and ICAM-1 in arterial wall are significantly suppressed by cisterna magna-injected SB203580 in experimental SAH of rabbits, which indicates that p38 MAPK takes part in the pathogenesis of CVS after SAH through the inflammatory response in arterial wall.