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。
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.
出处
《江苏医药》
CAS
北大核心
2013年第16期1877-1880,F0002,共5页
Jiangsu Medical Journal
基金
江苏大学人才引进科研启动基金(2006-20)
