大鼠脑缺血再灌注后半影区葡萄糖转运体3表达的变化(英文)  

Changes of rat penumbral glucose transporter-3 expression following cerebral ischemia-reperfusion injury

作　　者：李方成[1] 陶宗玉[2] 刘安民[1] 李军亮[1] 张蕲[3] 吴中华[1] 林吉惠[1] 

机构地区：[1]中山大学附属第二医院神经外科,广东省广州市510120 [2]泰安市中心医院,山东省泰安市271000 [3]华中科技大学同济医学院病理生理系,湖北省武汉市430030

出　　处：《中国临床康复》2005年第45期150-152,共3页Chinese Journal of Clinical Rehabilitation

基　　金：国家自然科学基金资助项目(39900048);广东省自然科学基金资助基目(010721)~~

摘　　要：背景:近年来的研究表明,缺血缺氧导致脑内代谢异常乃至能量衰竭,是引起脑组织损伤坏死的重要原因,可见能量代谢障碍是脑缺血再灌注损伤的中心问题。在脑的能量代谢中葡萄糖转运体3中发挥着重要作用。目的:观察大鼠局灶性脑缺血不同缺血时间和不同再灌注时间的脑梗死体积比、皮质半影区葡萄糖转运体3转录水平和蛋白水平的表达。设计:随机对照实验。单位:中山大学附属第二医院神经外科。材料:实验于2002-08/10在中山大学附属第二医院医学研究中心动物试验室完成。选择SD大鼠56只,随机分成3组:①缺血1h再灌注组28只。②缺血3h再灌注组24只。③假手术对照组4只。缺血1h再灌注组自缺血开始分别选取1,3,6,12,24,72h,1周7个时间点,每个时间点7只大鼠;缺血3h再灌注组除无1h时点外,其余时间点与缺血1h再灌注组相同,假手术对照组只作切口,不作插线。方法:用线栓法复制大鼠局灶性脑缺血模型,检测缺血中心区和缺血半影区脑梗死体积比;剥取缺血半影区皮质组织,采用反转录-聚合酶链反应测定葡萄糖转运体3mRNA水平的变化;用免疫组织化学方法半定量测定葡萄糖转运体3蛋白水平的变化。主要观察指标:①各组大鼠脑缺血再灌注后的脑梗死面积。②各组大鼠脑缺血再灌注后的葡萄糖转运体3mRNA表达水平的变化。③各组大鼠脑缺血再灌注后的葡萄糖转运体3蛋白水平表达的变化。结果:56只大鼠均进入结果分析。①脑缺血1h后再灌注组的脑梗死体积明显小于缺血3h再灌注组梗死体积。②葡萄糖转运体3mRNA及蛋白水平表达变化:葡萄糖转运体3自3h即开始升高,24h到达高峰,1周时仍高于假手术对照组;缺血3h再灌注组在3h有一下降点,然后升高,24h到高峰,1周时接近正常水平。葡萄糖转运体3蛋白水平的表达与mRNA相符合。结论:葡萄糖转运体3在缺血半影区的表达上调BACKGROUND： Recent researches indicate that ischemia and hypoxia can lead to abnormal brain metabolism and even energy failure, which is an important reason for brain damage and necrosis and identifies energy metabolism disorder as the key event in brain ischemia-reperfusion （IR） injury. Glucose transporter-3 plays the vital role in brain energy metabolism. OBJECTIVE： To observe the changes of cerebral infarct volume and glucose transporter-3 mRNA and protein expressions in cerebral cortical penumbra at different stages of focal cerebral ischemia and reperfusion in rats. DESIGN： Randomized controlled experiment. SETTING： Department of Neurosurgery, Second Hospital Affiliated to Sun Yat-sen University. MATERIALS： This experiment was conducted in the Animal Laboratory of Medical Research Center, Second Hospital Affiliated to Sun Yaten University between August and October 2002. Totally 56 SD rats were randomized into 3 groups which were subjected to （1） ischemia for 1 hour followed by reperfusion （n=28）, （2） ischemia for 3 hours followed by reperfusion （n=24）, and （3） sham operation （n=4）. The rats in the first group were subdivided into 7 subgroups for examination at 1, 3, 6, 12, 24, and 72 hours and 1 week after ischemia, with 7 rats in each subgroup; the rats in the second ischemia group were also subdivided in similar manner but without a 1 hour postischemic subgroup. The rats in the sham operation group only received the operation but without arterial occlusion. METHODS： Focal cerebral ischemia-reperfusion （IR） injury model was induced in the rats in the two ischemic groups by means of insertion of suture for arterial occlusion, and the ratio of central ischemic area to cerebral infarct volume in the ischemic penumbra was examined at the specified time points. Reverse transcription-PCR （RT-PCR） was used to detect the expression of glucose transporter-3 mRNA in the cerebral cortex in ischemic penumbra region, and semi-quantitative immunohistochemistry （I

关 键 词：脑缺血 再灌注 单糖转运蛋白质类 免疫组织化学 

分 类 号：R743.31[医药卫生—神经病学与精神病学]