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

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。

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

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).