中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2004年
16期
3176-3177
,共2页
张红%李琴%谭金强%宫钦爽%郭云良
張紅%李琴%譚金彊%宮欽爽%郭雲良
장홍%리금%담금강%궁흠상%곽운량
脑缺血/病理生理学%肌苷/治疗应用%内皮生长因子%基因表达
腦缺血/病理生理學%肌苷/治療應用%內皮生長因子%基因錶達
뇌결혈/병리생이학%기감/치료응용%내피생장인자%기인표체
背景:肌苷参与机体多方面的代谢过程,对缺血性脑损伤具有一定的保护作用,但其机制还没有彻底阐明.目的:研究肌苷对大鼠脑缺血再灌注后血管内皮生长因子(vascular endothelial growthfactor,VEGF)表达的影响,探讨肌苷的神经保护作用机制.设计:随机对照的实验研究.地点和材料:本实验在青岛大学医学院脑血管病研究所和山东省脑血管病防治重点实验室完成.成年健康雌性SD大鼠68只,体质量230~270 g,清洁级,由中国科学院上海实验动物中心提供.干预措施:成年健康雌性SD大鼠68只,应用线栓法建立SD大鼠大脑中动脉阻塞(MCAO)再灌注模型,随机分为治疗组32只和对照组32只,每组再随机分为缺血1.5 h再灌流2,6,12,24 h,2,3,7,14 d组(n=4),另外4只作假手术组.应用免疫组织化学方法检测脑缺血再灌流后脑组织VEGF的表达.结果:假手术组脑组织未见VEGF阳性表达.对照组在皮层区和纹状体区VEGF在脑缺血再灌注2 h开始表达,12 h达高峰,持续24 h,随即迅速降低.VEGF阳性细胞主要位于Ⅱ,Ⅲ,Ⅳ层神经元和血管内皮细胞,尤其神经细胞核周细胞浆和树突染色最深.肌苷治疗组VEGF表达于缺血再灌注2 h~2 d较对照组显著增高,经统计学处理,差异有非常显著性意义(t=3.78~22.62,P<0.01).结论:肌苷可上调脑缺血再灌注后VEGF的表达,可能是其缺血后神经保护作用的机制之一.
揹景:肌苷參與機體多方麵的代謝過程,對缺血性腦損傷具有一定的保護作用,但其機製還沒有徹底闡明.目的:研究肌苷對大鼠腦缺血再灌註後血管內皮生長因子(vascular endothelial growthfactor,VEGF)錶達的影響,探討肌苷的神經保護作用機製.設計:隨機對照的實驗研究.地點和材料:本實驗在青島大學醫學院腦血管病研究所和山東省腦血管病防治重點實驗室完成.成年健康雌性SD大鼠68隻,體質量230~270 g,清潔級,由中國科學院上海實驗動物中心提供.榦預措施:成年健康雌性SD大鼠68隻,應用線栓法建立SD大鼠大腦中動脈阻塞(MCAO)再灌註模型,隨機分為治療組32隻和對照組32隻,每組再隨機分為缺血1.5 h再灌流2,6,12,24 h,2,3,7,14 d組(n=4),另外4隻作假手術組.應用免疫組織化學方法檢測腦缺血再灌流後腦組織VEGF的錶達.結果:假手術組腦組織未見VEGF暘性錶達.對照組在皮層區和紋狀體區VEGF在腦缺血再灌註2 h開始錶達,12 h達高峰,持續24 h,隨即迅速降低.VEGF暘性細胞主要位于Ⅱ,Ⅲ,Ⅳ層神經元和血管內皮細胞,尤其神經細胞覈週細胞漿和樹突染色最深.肌苷治療組VEGF錶達于缺血再灌註2 h~2 d較對照組顯著增高,經統計學處理,差異有非常顯著性意義(t=3.78~22.62,P<0.01).結論:肌苷可上調腦缺血再灌註後VEGF的錶達,可能是其缺血後神經保護作用的機製之一.
배경:기감삼여궤체다방면적대사과정,대결혈성뇌손상구유일정적보호작용,단기궤제환몰유철저천명.목적:연구기감대대서뇌결혈재관주후혈관내피생장인자(vascular endothelial growthfactor,VEGF)표체적영향,탐토기감적신경보호작용궤제.설계:수궤대조적실험연구.지점화재료:본실험재청도대학의학원뇌혈관병연구소화산동성뇌혈관병방치중점실험실완성.성년건강자성SD대서68지,체질량230~270 g,청길급,유중국과학원상해실험동물중심제공.간예조시:성년건강자성SD대서68지,응용선전법건립SD대서대뇌중동맥조새(MCAO)재관주모형,수궤분위치료조32지화대조조32지,매조재수궤분위결혈1.5 h재관류2,6,12,24 h,2,3,7,14 d조(n=4),령외4지작가수술조.응용면역조직화학방법검측뇌결혈재관류후뇌조직VEGF적표체.결과:가수술조뇌조직미견VEGF양성표체.대조조재피층구화문상체구VEGF재뇌결혈재관주2 h개시표체,12 h체고봉,지속24 h,수즉신속강저.VEGF양성세포주요위우Ⅱ,Ⅲ,Ⅳ층신경원화혈관내피세포,우기신경세포핵주세포장화수돌염색최심.기감치료조VEGF표체우결혈재관주2 h~2 d교대조조현저증고,경통계학처리,차이유비상현저성의의(t=3.78~22.62,P<0.01).결론:기감가상조뇌결혈재관주후VEGF적표체,가능시기결혈후신경보호작용적궤제지일.
BACKGROUND: Inosine takes part in a lot of metabolic processes and has a protective effect on cerebral ischemic injury, but its mechanism is not known thoroughly.OBJECTIVE: To study the effect of inosine on expression of vascular endothelial growth factor(VEGF) in the cerebral tissue after cerebral ischemia reperfusion in rats, and to explore the neuroprotective mechanism of inosine.DESIGN: A randomized controlled basic research.SETTING and MATERIALS: This experiment was carried out at the Institute of Cerebrovascular Diseases, College of Medicine, Qingdao University and the Key Laboratory of Cerebrovascular Diseases of Shandong Province.Sixty-eight adult healthy female SD rats, weighting 230- 270 g, clearing grade, were purchased from Shanghai Experimental Animal Center of the Chinese Academy of Science.INTERVENTION: The models of ischemia/reperfusion in SD rats were established by middle cerebral artery occlusion(MCAO) with a nylon monofilament suture. The rats were randomly divided into the treatment groups 32cases and the control group 32 cases. Each group was divided into eight subgroups, which consisted of 4 rats at 2 hours, 6 hours, 12 hours, 24 hours, 2days , 3 days, 7 days and 14 days after reperfusion of MACO. The other 4cases served as sham-operated group. Immunohistochemical technique was used to investigate the dynamic changes of VEGF in cerebral tissue.RESULTS: There was no expression of VEGF in cerebral tissue of sham-operated group. The expression of VEGF occurred at 2 hours, peaked at 12-24 hours after reperfusion and then decreased rapidly in cortex and striatum in the control group. VEGF expressed mainly in neurons and endothelial cells in Ⅱ, Ⅲ, Ⅳ layers in cortex, especially colored mostly in the perinucleus cytoplasm and dendrites of neurons. In the treatment group, the level of VEGF expression was significantly higher than that in the control group at reperfusion 2 hours - 2 days( t = 3.78 - 22.62, P < 0.01 ).CONCLUSIONS: These results indicated that Inosine could protect cerebral tissue against hypoxic-ischemic injury after reperfusion of focal cerebral ischemia, whose role might be reflected by increasing the expression of VEGF.