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缺血预处理对局灶性脑缺血再灌注大鼠顶叶皮层bFGF表达的影响

ISSN号：1006-2947
期刊名称：解剖科学进展
时间：0
页码：52-56
语言：中文
分类：R743.31[医药卫生—神经病学与精神病学;医药卫生—临床医学]
作者机构：[1]中国医科大学基础医学院神经生物学教研室,辽宁沈阳110001, [2]中国医科大学附属盛京医院麻醉科,辽宁沈阳110003, [3]辽宁中医学院职业技术学院生理学教研室,辽宁沈阳110101
相关基金：国家自然科学基金（No.30670723,No.30570650,No.30800451,No.30700861,No.30872656）;辽宁省高等学校科研项目计划（No.2008850）;辽宁省自然科学基金（No.20052102）;沈阳市科学技术计划项目（No.1072033-1-00,No.1081266-9-00）
相关项目：白喉毒素受体介导大分子药物通过血肿瘤屏障效果和机制的研究

关键词：脑缺血预处理, 脑缺血再灌注, 碱性成纤维细胞生长因子, 大鼠, cerebral ischemic preconditioning, cerebral ischemia-reperfusion, bFGF, rat

中文摘要：

目的研究脑缺血预处理对大鼠局灶性脑缺血再灌注损伤及脑顶叶皮层碱性成纤维细胞生长因子（bFGF）表达的影响。方法线栓法阻塞32只大鼠大脑中动脉15min作为预处理，3天后线栓法制备大鼠大脑中动脉缺血模型，缺血2h再灌注24h后，缺血再灌注组32只。观察神经功能缺损程度、脑梗死体积、脑含水量、bFGF表达的变化。结果与对照组相比，脑缺血预处理组神经功能缺损评分明显降低（P〈0．01），TFC染色显示脑梗死体积明显减小（P〈0．01），缺血侧的脑水肿程度明显减轻（P〈0．01），免疫组化和Western blot检测表明脑顶叶皮层缺血周围组织bFGF表达水平明显升高（P〈0．01），阳性细胞以神经元和胶质细胞为主。结论预先给予短暂性脑缺血预处理可对脑缺血再灌注损伤起保护作用，bFGF过表达可能是其机制之一。

英文摘要：

Objective To investigate the effect of ischemic preconditioning on the brain damage and expression of basic fibroblast growth factor （bFGF） in focal cerebral ischemia-reperfusion rats. Methods Cerebral ischemic preconditioning for 15min was given by middle cerebral artery ccelusion（MCAO） and 3d later MCAO was occluded for 2h and reperfused for 24h by intraluminal suture in 32 rats. Ischemia-reperfusion model was made as control in 32 rats. The neurological deficit, infarct volume and brain water content were evaluated, and bFGF expression was determined by immunohistoehemistry and Western blot. Results Compared with control group, neurological deficit score was significantly decreased （P〈0.01）, infarct volume was reduced by TTC staining （P〈0.01） and brain edema was relieved （P〈0.01）, bFGF expression was increased in surrounding area of the ischemic region of the parietal lobe by immunohistochemistry and Western blot analysis （P〈0.01）, and the positive cells were primarily neurons and gliocytes in ischemic preconditioning group. Conclusion Cerebral ischemic preconditioning has protective effects against cerebral ischemic injury, bFGF overexpression may contribute to one of the protective mechanisms.

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