【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。更多还原

【Abstract】 Objective To investigate the possible mechanism of p38mitogen-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-injected 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-1in 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-6and ICAM-1in arterial wall are significantly suppressed by cisterna magna-injected SB203580in 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.更多还原