NF-κB、ICAM-1在实验性SAH后基底动脉壁上的表达变化

Expression of NF-κB and ICAM-1 on the basilar artery after experimental SAH

目的探讨免疫炎症反应在蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后脑血管痉挛(cerebral vasospasm,CVS)发病机制中的作用。方法应用新西兰家兔经枕大池二次注血制成SAH动物模型。在各相应时间点运用数字减影血管造影(digital subtraction angiography,DSA)、HE染色和免疫组化等方法,观察兔基底动脉管壁形态以及核转录因子kappaB(nuclear factor-kappaB,NF-κB)、细胞间粘附因子-1(intercellular adhesion molecule,ICAM-1)在管壁上表达的动态变化。结果在SAH后第3天基底动脉血管腔已开始狭窄,第7天达到高峰,之后狭窄渐减轻,14d时基本接近正常。SAH后3d NF-κB表达增加,5～7d表达持续在一个较高的水平,随后开始下降;ICAM-1表达变化趋势与NF-κB相似,但在表达高峰时相上稍迟于后者。结论NF-κB、ICAM-1在血管壁上的表达变化与CVS的发生时相密切相关,提示由其参与介导的血管壁炎症反应可能在CVS的发生和发展过程中起了重要的作用。

Objective To evaluate the possible effect of inflammatory reaction in the pathogenesis of CVS after SAH.Methods The ＂double-hemorrhage＂ model of vasospasm was performed by two injections of autologous aterial blood into the cisterna magna of Newzealand rabbits.We oberserved morphological changes and the rule of expression and activity of NF-κB and ICAM-1 in basilar artery（BA） walls by DSA,light microscope and immunohistochemistry.Results The ＂double-hemorrhage＂ model of vasospasm was succeeded to be made.The BA vasospasm was obvious on 3d after autologous aterial blood was first injected into the cisterna magna,and peaked on 7d,and then relieved.On 14d,there was almost no abnormality in the arterial wall.Upregulation of NF-κB expression started on 3d,became stronger on 5d to 7d,and then decreased.The upregulation of ICAM-1 expression in the BA walls was similar with NF-κB,but was a bit later to reach it＇s peak than NF-κB.Conclusions The results showed that the over-activation of NF-κB and ICAM-1 in BA positively correlated with the vasospasm.Inflammatory reaction in arterial walls mediated by NF-8κB may play a key role in the process of CVS after SAH.