论文部分内容阅读
目的探讨兔蛛网膜下腔出血(subarachnoid hemorrhage,SAH)脑血管痉挛(cerebral vasospasm,CVS)后丝裂原活化蛋白激酶p38(p38 Mitogen-activated kinase protein,p38MAPK)、核转录因子-κB(nuclear transcription fac-tor-κB,NF-κB)及细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)在海马的表达。方法将新西兰纯种健康级大白兔60只分为对照组(n=5)、生理盐水(NS)注射组(n=5)、SAH组(n=30)、干预组(n=20)。SAH组又分为SAH后1、3、5、7、9、11 d 6个亚组。干预组分为NS治疗组、ICAM-1单克隆抗体治疗组、NF-κB拮抗剂治疗组、p38MAPK抑制组4个亚组。枕大池二次注血制作兔SAH后CVS模型。分离海马,应用免疫组化观察海马p38MAPK、NF-κB及ICAM-1表达变化。结果 p38MAPK、NF-κB及ICAM-1在对照组和NS注射组的海马神经细胞上仅有微弱染色。伴随着血管腔痉挛的加重,ICAM-1的表达逐渐增强,第7天表达最为强烈;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。经拮抗剂治疗后,p38MAPK、NF-κB染色信号明显减弱,ICAM-1仅有微弱表达;经单克隆抗体治疗后,p38MAPK、NF-κB有较强表达,ICAM-1有微弱表达。结论兔SAH及CVS后海马神经细胞存在着与上述因子相关的免疫炎症反应。抑制上述因子的表达,可以较好地控制损伤脑组织的免疫炎症反应。
Objective To investigate the expression of p38 mitogen activated protein kinase (p38) and nuclear transcription factor-κB (p38) in rabbits after subarachnoid hemorrhage (SAH) cerebral vasospasm (CVS) fac-tor-κB, NF-κB and intercellular adhesion molecule-1 (ICAM-1) in the hippocampus. Methods Sixty New Zealand purebred healthy rabbits were divided into control group (n = 5), saline injection group (n = 5), SAH group (n = 30) and intervention group (n = 20). The SAH group was divided into six subgroups after 1,3,5,7,9 and 11 days after SAH. Interventions were NS treatment group, ICAM-1 monoclonal antibody treatment group, NF-κB antagonist treatment group, p38MAPK inhibition group 4 subgroups. CVS model of rabbits with SAH produced by secondary injection of occipital large pool. The hippocampus was separated and the expression of p38MAPK, NF-κB and ICAM-1 were detected by immunohistochemistry. Results p38MAPK, NF-κB and ICAM-1 were only weakly stained in the hippocampal neurons of the control and NS injection groups. With the aggravation of vasospasm, the expression of ICAM-1 gradually increased and the expression was most intense on the 7th day. The expression of p38MAPK and NF-κB tended to increase gradually, but the expression was stronger on the 5th day and then gradually decreased. After antagonist treatment, the signal of p38MAPK and NF-κB staining was significantly weakened, while the expression of ICAM-1 was only weakly expressed. After treatment with monoclonal antibody, p38MAPK and NF-κB were strongly expressed and ICAM-1 was weakly expressed. Conclusions There is immune-inflammatory reaction in hippocampal neurons after SAH and CVS in rabbits. Inhibition of the expression of these factors, can better control the damage of brain immune immune response.