摘要
目的:探讨脑出血后炎症反应机制及核因子-κB(NF-κB)与细胞间粘附分子-1(ICAM-1)间表达的关系。方法:建立大鼠脑出血模型及过氧化氢损伤大鼠脑微血管内皮细胞的模型,分别采用免疫组化、原位杂交、免疫细胞化学及Western blotting方法观察NF-κB和ICAM-1的表达。结果:大鼠脑出血后NF-κB及ICAM-1表达均增强,ICAM-1的表达高峰(1 d)先于NF-κB(4 d),但在体外实验中,过氧化氢损伤后即刻大鼠脑微血管内皮细胞中NF-κB表达即增加,2 h后ICAM-1表达也上调,NF-κB的抑制剂吡咯烷二硫氨基甲酸(PDTC)可下调NF-κB及ICAM-1表达。结论:在活性氧损伤中NF-κB作为ICAM-1的活化因子,可上调ICAM-1表达,但在脑出血这一复杂的病理生理变化中,尚有其它因素参与对NF-κB及ICAM-1表达的调控。
AIM : To discuss the possible mechanism of the inflammation after intracerebral hemorrhage (ICH) and the relationship of nuclear factor - kappa B ( NF - κB) and intercellular adhesion molecule - 1 ( ICAM - 1 ). METHODS : The expression of NF - κB and ICAM - 1 were detected by immunohistochemistry, in situ hybridization, immunocytochemistry and Western blotting techniques in rat brain of experimental ICH and cerebral microvascular endothelial cells (RCMECs) injured by hydrogen peroxide. RESULTS: The expression of NF - κB p65 and ICAM - 1 were up - regulated in rat brain after ICH. The ICAM - 1 reached the peak at 1 day while the NF - κB at 4th day. NF - κB p65 expressed remarkably in cultured RCMECs immediately after injured by hydrogen peroxide, while ICAM - 1 expressed remarkably 2 hours later. PDTC, an inhibitor of NF - κB, down - regulated the expression of NF - κB and ICAM - 1. CONCLUSION: NF - κB induces the expression of ICAM - 1 in RCMECs injured by reactive oxygen species (ROS).
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2007年第4期693-698,共6页
Chinese Journal of Pathophysiology
基金
国家中医药管理局资助项目(No.2000-J-B-03)
关键词
脑出血
胞间粘附分子1
NF—κB
Cerebral hemorrhage
Intercellular adhesion molecule - 1
NF - kappa B