脑溢安对过氧化氢损伤大鼠脑微血管内皮细胞NF-κB、IκB和ICAM-1表达的影响  

PROTECTIVE EFFECTS OF NAOYI'AN ON RATS' CEREBRAL MICROVASCULAR ENDOTHELIAL CELLS INJURY CAUSED BY HYDROGEN PEROXIDE

作　　者：智屹惠[1] 黎杏群[2] 李彤 万赛英[2] 唐涛[2] 

机构地区：[1]浙江省中医院,杭州310000 [2]中南大学湘雅医院,长沙410008 [3]浙江大学医学院第一附属医院,杭州310000

出　　处：《中国中医药科技》2009年第2期94-97,79,共4页Chinese Journal of Traditional Medical Science and Technology

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。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.

关 键 词：脑出血后炎症反应/中医药疗法 @脑溢安/治疗应用 内皮 血管 血清药理学 大鼠 

分 类 号：R285.5[医药卫生—中药学]