CAJ | 학술논문

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1 h再灌注组28只.②缺血3 h再灌注组24只.③假手术对照组4只.缺血1 h再灌注组自缺血开始分别选取1,3,6,12,24,72 h,1周7个时间点,每个时间点7只大鼠;缺血3 h再灌注组除无1 h时点外,其余时间点与缺血1 h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3 mRNA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3 mRNA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1 h后再灌注组的脑梗死体积明显小于缺血3 h再灌注组梗死体积.②葡萄糖转运体3 mRNA及蛋白水平表达变化:葡萄糖转运体3自3 h即开始升高,24 h到达高峰,1周时仍高于假手术对照组;缺血3 h再灌注组在3 h有一下降点,然后升高,24 h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,可能是机体对缺血再灌注的保护性反应. 揹景:近年來的研究錶明,缺血缺氧導緻腦內代謝異常迺至能量衰竭,是引起腦組織損傷壞死的重要原因,可見能量代謝障礙是腦缺血再灌註損傷的中心問題.在腦的能量代謝中葡萄糖轉運體3中髮揮著重要作用.目的:觀察大鼠跼竈性腦缺血不同缺血時間和不同再灌註時間的腦梗死體積比、皮質半影區葡萄糖轉運體3轉錄水平和蛋白水平的錶達.設計:隨機對照實驗.單位:中山大學附屬第二醫院神經外科.材料:實驗于2002-08/10在中山大學附屬第二醫院醫學研究中心動物試驗室完成.選擇SD大鼠56隻,隨機分成3組:①缺血1 h再灌註組28隻.②缺血3 h再灌註組24隻.③假手術對照組4隻.缺血1 h再灌註組自缺血開始分彆選取1,3,6,12,24,72 h,1週7箇時間點,每箇時間點7隻大鼠;缺血3 h再灌註組除無1 h時點外,其餘時間點與缺血1 h再灌註組相同,假手術對照組隻作切口,不作插線.方法:用線栓法複製大鼠跼竈性腦缺血模型,檢測缺血中心區和缺血半影區腦梗死體積比;剝取缺血半影區皮質組織,採用反轉錄-聚閤酶鏈反應測定葡萄糖轉運體3 mRNA水平的變化;用免疫組織化學方法半定量測定葡萄糖轉運體3蛋白水平的變化.主要觀察指標:①各組大鼠腦缺血再灌註後的腦梗死麵積.②各組大鼠腦缺血再灌註後的葡萄糖轉運體3 mRNA錶達水平的變化.③各組大鼠腦缺血再灌註後的葡萄糖轉運體3蛋白水平錶達的變化.結果:56隻大鼠均進入結果分析.①腦缺血1 h後再灌註組的腦梗死體積明顯小于缺血3 h再灌註組梗死體積.②葡萄糖轉運體3 mRNA及蛋白水平錶達變化:葡萄糖轉運體3自3 h即開始升高,24 h到達高峰,1週時仍高于假手術對照組;缺血3 h再灌註組在3 h有一下降點,然後升高,24 h到高峰,1週時接近正常水平.葡萄糖轉運體3蛋白水平的錶達與mRNA相符閤.結論:葡萄糖轉運體3在缺血半影區的錶達上調,可能是機體對缺血再灌註的保護性反應.
배경:근년래적연구표명,결혈결양도치뇌내대사이상내지능량쇠갈,시인기뇌조직손상배사적중요원인,가견능량대사장애시뇌결혈재관주손상적중심문제.재뇌적능량대사중포도당전운체3중발휘착중요작용.목적:관찰대서국조성뇌결혈불동결혈시간화불동재관주시간적뇌경사체적비、피질반영구포도당전운체3전록수평화단백수평적표체.설계:수궤대조실험.단위:중산대학부속제이의원신경외과.재료:실험우2002-08/10재중산대학부속제이의원의학연구중심동물시험실완성.선택SD대서56지,수궤분성3조:①결혈1 h재관주조28지.②결혈3 h재관주조24지.③가수술대조조4지.결혈1 h재관주조자결혈개시분별선취1,3,6,12,24,72 h,1주7개시간점,매개시간점7지대서;결혈3 h재관주조제무1 h시점외,기여시간점여결혈1 h재관주조상동,가수술대조조지작절구,불작삽선.방법:용선전법복제대서국조성뇌결혈모형,검측결혈중심구화결혈반영구뇌경사체적비;박취결혈반영구피질조직,채용반전록-취합매련반응측정포도당전운체3 mRNA수평적변화;용면역조직화학방법반정량측정포도당전운체3단백수평적변화.주요관찰지표:①각조대서뇌결혈재관주후적뇌경사면적.②각조대서뇌결혈재관주후적포도당전운체3 mRNA표체수평적변화.③각조대서뇌결혈재관주후적포도당전운체3단백수평표체적변화.결과:56지대서균진입결과분석.①뇌결혈1 h후재관주조적뇌경사체적명현소우결혈3 h재관주조경사체적.②포도당전운체3 mRNA급단백수평표체변화:포도당전운체3자3 h즉개시승고,24 h도체고봉,1주시잉고우가수술대조조;결혈3 h재관주조재3 h유일하강점,연후승고,24 h도고봉,1주시접근정상수평.포도당전운체3단백수평적표체여mRNA상부합.결론:포도당전운체3재결혈반영구적표체상조,가능시궤체대결혈재관주적보호성반응.
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 Yat-sen 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 72hours 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 (IHC) employed to detect the level of glucose transporter-3 protein.MAIN OUTCOME MEASURES: Cerebral infarct volume after IR injury, changes of transporter-3 mRNA and protein expressions after IR injury.RESULTS: Totally 56 rats were used in this experiment and all entered result analysis. The post-IR cerebral infarct volume was obviously smaller in 1-hour ischemia group than in 3-hour ischemia group. Glucose transporter-3 mRNA expression began to increase 3 hours after ischemia in 1-hour ischemia group, reaching the peak level at 24 hours and still mainrained higher level than that of the sham operation 1 week; in 3-hour ischemia group, the mRNA expression was slightly decreased at 3 hours but began to increase afterwards till reaching the peak level at 24 hours, followed then by recovery of normal level at 1 week. The changes in glucose transporter-3 protein and mRNA expressions followed almost the same pattern.CONCLUSION: Glucose transporter-3 expression is up-regulated in the ischemic penumbra region, possibly as a protective response to cerebral IR injury.