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目的探讨兔蛛网膜下腔出血(SAH)后丝裂原活化蛋白激酶p38(p38MAPK)、核转录因子-κB(NF-κB)及细胞间粘附分子-1(ICAM-1)在脑血管痉挛(CVS)发病机制中的作用及其相互间内在关系。方法将新西兰纯种健康级大白兔92只分为正常组(n=10)、对照组(n=10)、SAH组(n=72),SAH组又分为SAH后1、3、5、7、9、11d6个亚组。枕大池二次注血制作兔SAH后CVS模型。分离兔基底动脉(BA),应用形态学观察、免疫组化和原位杂交等方法,观察兔BA管径、血管壁上p38MAPK、NF-κB及ICAM-1表达的动态变化及其与CVS的关系。结果在SAH后第3天,BA管腔出现狭窄,第5天时狭窄明显,第7天狭窄最为明显。伴随着血管腔管径的变化,血管壁上ICAM-1的表达逐渐增强,第7天时表达最为强烈;p38MAPK、NF-κB的表达也呈逐渐增强的趋势,但在第5天时表达最为强烈,之后逐渐降低。p38MAPK、NF-κB与ICAM-1在蛋白质和mRNA水平上的强烈表达有时程上的差别。结论在CVS的早期即出现的p38MAPK、NF-κB高表达以及之后出现的ICAM-1高表达,均提示存在由p38MAPK、NF-κB调控的ICAM-1介导的痉挛血管壁的炎症反应,这一级联反应在CVS的发生和发展过程中起了重要作用。
Objective To investigate the expression of p38MAPK, NF-κB and ICAM-1 in patients with cerebral vasospasm after subarachnoid hemorrhage (SAH) (CVS) pathogenesis and its relationship with each other. Methods Ninety-two New Zealand purebred healthy white rabbits were divided into normal group (n = 10), control group (n = 10) and SAH group (n = 72) 7,9,11 d6 subgroups. CVS model of rabbits with SAH produced by secondary injection of occipital large pool. The basilar artery (BA) of rabbits was isolated and the changes of BA diameter, the expressions of p38MAPK, NF-κB and ICAM-1 on the vascular wall were observed by morphological observation, immunohistochemistry and in situ hybridization. relationship. Results On the 3rd day after SAH, the lumen of BA was stenotic, the stenosis was obvious on the fifth day and the stenosis was most obvious on the seventh day. The expression of ICAM-1 on the vascular wall gradually increased with the change of the diameter of the vascular lumen, and the expression was most intense on the 7th day. The expression of p38MAPK and NF-κB tended to increase gradually, After gradually reduced. There is a time-course difference in the strong expression of p38 MAPK, NF-κB and ICAM-1 at the protein and mRNA levels. Conclusions The high expression of p38MAPK and NF-κB in early stage of CVS and the subsequent expression of ICAM-1 in the early stage of CVS suggest the existence of ICAM-1-mediated inflammatory reaction in splenic vessel wall regulated by p38MAPK and NF-κB A cascade reaction plays an important role in the occurrence and development of CVS.