NF-κB及ICAM-1在脑出血大鼠及过氧化氢损伤大鼠脑微血管内皮细胞中的表达

The expression of NF-κB and ICAM-1 in rat brain of experimental intracerebral hemorrhage and cerebral microvascular endothelial cells injured by hydrogen peroxide

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）.