局灶性脑缺血预处理对胶质纤维酸性蛋白表达的影响  

Expression of glial fibrillary acidic protein(GFAP) after focal cerebral ischemic preconditioning in rat

作　　者：舒勤奋[1] 刘小利[1] 倪娇娜[1] 吴炯[1] 金煜[1] 李雅国[1] 

机构地区：[1]浙江医院神经内科,杭州310013

出　　处：《浙江医学》2008年第7期696-697,722,共3页Zhejiang Medical Journal

摘　　要：目的观察局灶性脑缺血预处理(IP)对胶质纤维酸性蛋白(GFAP)表达的影响,探讨GFAP与脑缺血耐受(IT)的关系及可能的内源性神经保护机制。方法SD大鼠随机分为IP组、大脑中动脉阻塞(MCAO)组、对照组。动物模型的制备参照有关文献。采用TTC染色测定脑梗死体积,光镜下观察脑组织病理改变,免疫组织化学染色和图像分析评价各组GFAP的表达。结果IP组脑梗死体积较MCAO组明显减小(P<0.05),光镜下病理改变减轻,GFAP表达水平较MCAO组和对照组升高(均P<0.05)。结论IP能够提供脑保护,诱导脑IT的形成。其可能的机制之一是通过促进星形胶质细胞的活化,启动内源性的神经保护机制而加强了对再次缺血损伤的保护作用。Objective To investigate the expression of glial fibnllary acidic protein（GFAP）in the ischemic tolerance induced by focal cerebral ischemic preconditioning. Methods Ischemic preconditioning （IP） was induced by intraluminal filament middle cerebral artery for 10 min. Middle cerebral artery occlusion （MCAO） was induced by intraluminal filament for 2h, 72h after IP. Thirty SD rats were randomly divided into 3 groups （10 in each group）： control group did not receive any treatment, SS＋MCAO group only received 2h MCAO followed by 22h reperfusion and sham surgery; IP＋MCAO group received 2h MCAO followed by 22h reperfusion with IP. At end of perfusion the infarct volume was measured, histopathology with HE staining was examined under microscopy, the expression of GFAP was detected by immunohistochemistry in each group. Results The infarct volume of IP＋MCAO group was significantly less than that of SS＋MCAO （P〈0.05）. The pathological change was moderate in the brain of IP ＋MCAO group than that of （SS＋MCAO） group. The rate of GFAP positive cells in the brain of SS＋MCAO group was significantly lower than that in the IP＋MCAO group （P〈0.05）. Conclusion Focal cerebral ischemic preconditioning can protect brain from ischemic damage and induce ischemic tolerance, which might be associated with upregulation of GFAP expression.

关 键 词：缺血预处理 缺血耐受 胶质纤维酸性蛋白 大脑中动脉阻塞 

分 类 号：R743.3[医药卫生—神经病学与精神病学]