核转录因子κB在大鼠全脑缺血耐受中的表达及意义  

The expression and significance of nuclear factor kBin the rats with cerebral ischemic tolerance.

作　　者：田代实[1] 刘俊丽[2] 王光海[1] 郭国际[1] 占克斌[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院神经内科,武汉430030 [2]华中科技大学同济医学院附属同济医院肿瘤科,武汉430030

出　　处：《脑与神经疾病杂志》2003年第6期321-323,共3页Journal of Brain and Nervous Diseases

摘　　要：目的:探讨核转录因子кB(NFкB)在大鼠全脑缺血耐受中的表达及其意义。方法:建立大鼠四血管闭塞的全脑缺血耐受模型,将实验动物随机分为6组:缺血预处理组(IP),DTTC(NFкB的特异性抑制剂)加缺血预处理组(IP^(DTTC)),缺血再灌注组(I/R),缺血预处理加缺血再灌注组(IP+I/R),DTTC加缺血预处理组加缺血再灌注组(IP^(DTTC)+I/R),假手术组(sham)。各组行海马神经元计数,并用凝胶电泳迁移率改变分析法检测NFкB活性。结果:IP和I/R中NFкB均被激活;IP+I/R组与I/R组相比,神经元计数明显增高;DTTC可抑制NFкB活性,也抑制IP的神经保护作用。结论:IP可通过激活NFкB发挥神经保护作用。Objective: To study the expression and significance of nuclear factor κB(NBκB)in the rats with cerebral ische-mic tolerance. Methods: Rate were randomly allocated to one of six groups;①sham operation(sham) ; ②3min ischemic preconditioning (IP) ;③Ip in the presence of DTTC, a specific NFκB inhibitor(IPDTTC ; ④10min ischemia and reperfusion(I/R) ;⑤IP followed by I/R (IP + I/R) ; ⑥IP in the presence of DTTC followed by I/R( IPDTTC+I/R) . The neuronal density of hippocampus and NFκB activation were determined. Results: In preconditioned rats( IP + I/R) , the neuronal density of hippocampus was increased significantly compared with both I/R alone and IPDTTC+ I/R groups( P < 0. 01). Electrophoretic mobility shift assays (EMSA) showed NFκB activation with IP that was blocked by DTTC. I/R alone and IPDTTC+I/R groups showed NFκB acitva-tion with I/R that was absent in preconditioned rats. Conclusions; The cytoprotective effects induced by IP require activation of NFκB.

关 键 词：核转录因子ΚB 脑缺血 表达 凝胶电泳迁移率改变分析 缺血耐受 

分 类 号：R743[医药卫生—神经病学与精神病学]