I-κBα在大鼠局灶性脑缺血再灌注后的作用  

Role of I-κBα in focal cerebral ischemic reperfusion

作　　者：姚小梅[1] 王纪佐[1] 朱学良[1] 

机构地区：[1]天津医科大学病理生理教研室,300070

出　　处：《中华神经医学杂志》2005年第3期238-240,共3页Chinese Journal of Neuromedicine

基　　金：天津市高等学校科技发展基金项目(20030123)

摘　　要：目的研究I-κBα在大鼠脑缺血再灌注损伤后作用的蛋白表达的时间和空间分布特点.方法应用Western Blot方法检测对照组及脑缺血2 h再灌注不同时程组(15 h、24 h、48 h)I-κBα蛋白表达水平,并用免疫组化技术研究I-κBα在脑缺血再灌注后作用的空间分布. 结果Western Blot研究发现I-κBα在对照组表达很低,于脑缺血2 h再灌注后15～24 h达到高峰,48 h始有所下降(P＜0.01).免疫组化研究发现:在半暗带的神经元、脑室壁和脉络丛及小血管内皮细胞均有I-κBα的阳性表达.结论由I-κBα介导的NF-κB激活和抑制通路在局灶性脑缺血再灌注损伤的半暗带神经元的存活和血脑屏障中起重要作用.如能在一恰当的时间段内使用合成的I-κBα来抑制NF-κB的激活,可能是一潜在的保护脑组织的治疗途径.Objective To investigate the mechanism of I-κBα action in cerebral ischemic reperfusion by determining I-κBα protein levels and probing into its distribution features in its temporal and spatial expression. Methods I-κBα protein levels in cerebral ischemic reperfusion in the sham group and the experimental groups at 15 h, 24 h and 48 h were detected by Western-blot method and the spacial distribution of I-κBα were studied by paraffin embedded immunocytochemistry. Results It was showed I-κBα was expressed at a very low level in the sham group, but it upregulated peaking at 15~24 h after ischemic reperfusion, and then began to decline at 48 h (P<0.01). Immunohistochemistry showed the positive expression of I-κBα in neurons of penumbra, endothelium of small vessels, ventricle ependymal epithelium and choroid plexus. Conclusion The I-κBα-mediated NF-κB-actived and -inbibited passagway plays an important role in both the survival of neurons of penumbra and blood brain barrier in focal cerebral ischemic reperfusion. If synthesized I-κBα can be used to inhibit the activation of NF-κB at an appropriate time span following cerebral ischemic reperfusion, it might be possible to develop a potential protecting treatment.

关 键 词：I-ΚBΑ 局灶性脑缺血再灌注损伤 大鼠 Western NF-ΚB激活 空间分布特点 蛋白表达水平 免疫组化技术 半暗带神经元 血管内皮细胞 Blot 研究发现 方法应用 血脑屏障 阳性表达 后作用 对照组 时间段 脉络丛 脑室壁 脑组织 

分 类 号：R743[医药卫生—神经病学与精神病学]