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机构地区:[1]内蒙古医学院附属医院神经外科,内蒙古呼和浩特010050
出 处:《内蒙古医学院学报》2009年第4期361-366,共6页Acta Academiae Medicinae Neimongol
基 金:内蒙古自治区卫生厅学科建设重点资助科研项目(2005077);内蒙古自治区自然科学基金资助项目(2008)
摘 要:目的:研究脑缺血再灌注损伤后脑红蛋白(NGB)在大脑皮质和海马区的表达变化。方法:改良ZeaLonga线栓法制备W istar大鼠大脑中动脉闭塞/再灌注模型(MCAO/R),在缺血2h后随机分为1h、4h、8h、16h、32h、64h和128h再灌注组和假手术组。采用神经功能评价、TTC染色、脑梗死体积测定、光镜HE检测等方法对不同组大鼠予以评价。采用免疫组化染色结合阳性细胞计数的方法,检测脑缺血再灌注损伤不同时间点大鼠脑组织梗死中心区和半暗带区NGB的表达变化。结果:大鼠脑缺血再灌注损伤后,大脑皮质的NGB蛋白表达损伤后呈现出先上升后下降的趋势,而非缺血侧对称区域皮质阳性表达不随时间变化。海马区NGB表达则呈持续减少的趋势。病理学检测显示海马区神经细胞损伤程度较大脑皮质区严重。结论:不同脑区对缺血性损伤的耐受性差异可能与NGB表达水平有关。NGB表达上调可能对脑缺血再灌注损伤具有保护作用。Objective:To observe the expression changes of neuroglobin(NGB) in cerebral cortex and hippocampus in wistar rats with middle cerebral artery ischemia-reperfusion injury.Methods:The middle cerebral artery occlusion(MCAO,for 2 hours) /reperfusion model in rats(MCAO/R group) was established by the modified suture-occluded method of Zea Longa.Then they were randomly divided into groups of reperfusion for 1h,4h,8h,16h,32h,64h and 128h and sham group.The methods of nerve function evaluation,TTC staining,infarct size estimation,detection with light microscope were used to evaluate the MCAO/R rat models at different time points,analysed the expression change of NGB in the center and the periphery of infarcts at different time points by immunohistochemical methods combined with computer-assisted image analysis.Results:The expression changes of NGB expression were different in cerebral cortex and in the hippocampus.The expression of NGB appeared increasing originally and decreasing later in the cerebral cortex,however the active expression wasn't change according to the changes of time.The expression of NGB appeared decreasing in the hippocampus.The pathological results showed that the injuried-deghee in the hippocampus was seriouser than in the cerebral artery.Conclusion:The endurance difference of ischemic injury may be associated with the expression of NGB in different area.The increased expression of NGB in the brain after ischemia-reperfusion may response to ischemic damage.
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