【摘要】 目的:探讨脑溢安对脑出血的保护作用机制。方法:建立过氧化氢损伤大鼠脑微血管内皮细胞模型,并用脑溢安血清及吡咯烷二硫氨基甲酸(Pyrrolidine dithiocarbamate,PDTC)加以干预,采用免疫细胞化学及Western blot方法观察核因子(NF-κB)、κB抑制蛋白(IκB)和细胞间黏附分子-1(ICAM-1)的表达。结果:过氧化氢损伤后即刻大鼠脑微血管内皮细胞中NF-κB及IκBα表达即增加,2小时后ICAM-1表达也上调,脑溢安及PDTC均可下调NF-κB及ICAM-1表达,上调IκB表达,免疫细胞化学及Westernblot观察到的结果一致。结论:脑微血管内皮细胞活性氧损伤后,NF-κB作为活化因子参与ICAM-1的调控;抑制NF-κB及ICAM-1的活性,减轻炎症反应,可能是脑溢安对脑出血的保护机制之一。更多还原

【Abstract】 Objective:To discuss the possible mechanism of naoyi’an to lessen the inflammation after intracerebral hemorrhage(ICH). Methods: Models with cerebral microvascular endothelial cells(CMECs) injury were induced by hydrogen peroxide, serum of containing naoyi’an and control medicine-pyrrolidine dithiocarbamate were given respectively to intervene. The expressions of nuclear factor-kappa B(NF-κB),inhibitor κB(IκBα) and intercellular adhension molecule-1(ICAM-1) in rats’ cerebral microvascular endothelial cells were determined by immunocytochemistry and Western blot technique . Results:The expressions of NF-κB and IκBα in CMECs were elevated immediately after injured by hydrogen peroxide,the expression of ICAM-1 was increased obviously 2 hours later.Naoyi’an and pyrrolidine dithiocarbamate could down-ragulate the expressions of NF-κB and ICAM-1, up-regulate the expression of IκBα, the results of immunocytochemistry and Western blot examinations were the same. Conclusion:Naoyi’an can lesen intracerebral hemorrhage injury, restraining the activity of NF-κB and ICAM-1 to lessen inflammation maybe one of its mechanism.更多还原