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高血脂对大鼠脑缺血再灌注损伤后海马内胶质纤维酸性蛋白表达的影响 被引量:3

Effect of hyperlipemia on GFAP expression in the hippocampus after cerebral ischemic-reperfusion injury in rats~
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摘要 目的:研究高血脂对大鼠脑缺血再灌注后海马CA4区内星形胶质细胞表达胶质纤维酸性蛋白(GFAP)的影响。方法:高脂饮食建立高血脂模型。以线栓法制作大鼠大脑中动脉阻塞的局灶性脑缺血再灌注模型,采用免疫组织化学和蛋白印迹与神经行为相结合的方法,观测缺血再灌注侧大脑海马CA4区内星形胶质细胞GFAP的表达和神经功能的变化。结果:在相同时间点内与假手术组比较,两组脑缺血再灌注组的星形胶质细胞数量均增多,GFAP的表达均增高;与脑缺血再灌注组比较,高血脂合并脑缺血再灌注组的星形胶质细胞数量减少,胞体较小,突起也少而细,GFAP的表达减少。结论:脑缺血再灌注损伤后星形胶质细胞的数量、形态以及GFAP的表达呈动态变化。 Objective: To observe the effect of hyperlipemia on glial fibrillary acidic protein (GFAP) expression in the hippocampus CA4 in rats after ischemiareperfusion in the brain. Methods: Application of highfat diet produced lipid model. The focal cerebral ischemicreperfusion model was established with thread embolism of the middle cerebral artery. Immunohisto chemistry, Western blot and neurobehavioral evaluation were used to examine the expression of GFAP in the hippocampus CA4 in the side of cerebral ischemia reperfusion and neurological function disorders. Results: Compared with shamoperation group, the number of astrocyte and the expression of GFAP were increased in both cerebral ischemia reperfusion groups in the same time point. Compared with cerebral ischemia reperfusion group, the expression of GFAP was decreased, the population of positive astrocyte declined, cell body was small and process was slender in hyperlipemia with cerebral ischemia- reperfusion group. Conclusion: After cerebral ischemia reperfusion, the number and shape of astrocyte and the expression of GFAP present dynamic changes.
出处 《解剖学杂志》 CAS CSCD 北大核心 2011年第6期766-769,共4页 Chinese Journal of Anatomy
基金 山西省高校科技研究开发项目(200613049)
关键词 胶质纤维酸性蛋白 星形胶质细胞 高血脂 脑缺血再灌注 glial fibrillary acidic proteim astrocyte high blood lipids cerebral ischemia-reperfusion
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  • 1张志军,吴利平,万群,江文.缺血再灌注对大鼠神经元与星形胶质细胞的影响[J].神经解剖学杂志,2005,21(6):611-614. 被引量:7
  • 2杨佳丹,董志.脑缺血再灌注损伤的病因学研究进展[J].中国康复医学杂志,2006,21(10):935-938. 被引量:21
  • 3任秀君,马惠芳,王晓宁,洪银珠,施昱丞,图娅.电针对高血脂合并脑缺血大鼠血脂及神经生长因子影响的实验研究[J].针刺研究,2007,32(1):24-28. 被引量:34
  • 4Orlowski P, Chappell M, Park C S, et al. Modelling of pH dynamics in brain cells after stroke[J]. Interface Focus, 2011,1 (3) : 408-416.
  • 5van den Tweel E R, Kavelaars A, Lomba_rdi M S, et al. Bilateral molecular changes in a neonatal rat model of unilateral hypoxic- isehemie brain damage[J]. Pediatr Res, 2006,59(3): 434-439.
  • 6E1Ali A, Doeppner T R, Zechariah A, et al. Increased blood- brain barrier permeability and brain edema after focal cerebral ischemia induced by hyperlipidemia: role of lipid peroxidation and calpain-1/2, matrix metalloproteinase-2/9, and RhoA overactiva- tion[J]. Stroke, 2011,42(11): 3238-3244.
  • 7Longa E Z, Weinstein P R, Carlson S, et al. Reversible middle cerebral artery occlusion without caranieetomy in rats[J]. Stroke, 1989,20(1) : 84-91.
  • 8Swanson R A, Morton M T, Tsao-Wu G, et al. A semiautomated method for measuring brain infarct volume[J]. J Cereb Blood Flow Metab, 1990,10(2): 290-293.
  • 9Won S J, Kim D Y, Gwag B J. Cellular and molecular pathway of isehemic neuronal death[J]. J Biochem Mol Biol, 2002,35 (1) : 67-86.
  • 10Sprick M R, Walczak H. The interplay between the Bct-2 family and death receptor-mediated apoptosis[J]. Biochim Biophys Acta, 2004,1644(2-3) : 125-132.

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