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行为学训练对局灶性脑缺血大鼠脑组织STAT1蛋白表达的影响 被引量:1

Effect of behavior training on the expression of STAT1 in cerebral tissue during focal cerebral ischemia in rats
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摘要 研究大鼠脑缺血再灌注后对信号转导子和转录激动子1(signal transducers and activators of transcription 1,STAT1)表达的影响,探讨穿梭箱行为学训练和碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)对脑组织缺血再灌注神经元STAT1的调节作用及机制。方法将96只Wistar大鼠随机分为训练1 d、3 d、7 d、14 d组;bFGF 1 d、3 d、7 d、14 d组;缺血再灌注1 d、3 d、7 d、14 d组及正常对照1 d、3 d、7 d、14 d组,每组6只。应用线栓法制作大鼠局灶性脑缺血再灌注模型,对不同组大鼠进行神经功能评分,训练组于造模1 d后开始给予穿梭箱训练,采用免疫组化检测不同时间点大脑皮质内STAT1的表达。结果正常对照组大鼠大脑皮质内STAT1少量的表达,造模后高于正常对照组,训练组及bFGF组大脑皮质内STAT1阳性表达较缺血再灌注组明显减少。结论穿梭箱训练及bFGF下调脑缺血诱导的STAT1表达,对脑缺血再灌注大脑皮质神经元的具有保护作用。 Objective To investigate the expression of signal transducers and activators of transcriptionl (STAT1) in the cortex after cerebral ischemia and reperfusion in rats, explore the regulative effects and mechanism of Behavior Training and basic fibroblast growth factor (bFGF) to STAT1 on brain tissue. Methods 96 wistar rats were randomized into ld, 3d, 7d, 14d training groups, ld, 3d, 7d, 14d bFGF groups, ld, 3d, 7d, 14d ischemia and reperfusion groups and control group.Behavior training were performed at 1st day after the infarction. The model of middle cerebral arteries occlusion (MCAO) were performed with intraluminal filament blockade, the expression of STAT1 in cortex was detected with immunohistochemical method at different points of time. Results The expression of STAT1 was certain in the normal cortex of rats. The expression of STAT1 increased after model group. However, the expression of STAT1 had obviously decreased in training groups and bFGF groups compared with that in ischemia and reperfusion groups. Conclusion The results indicate that training groups and bFGF groups participate in the regulation of expression of STAT1 in ischemic neurons.
出处 《解剖学研究》 CAS 2013年第2期100-103,共4页 Anatomy Research
基金 沈阳市科学计划项目课题(F11-262-9-17) 辽宁省教育厅科学研究计划资助项目(L2010546)
关键词 脑缺血 行为学训练 碱性成纤维细胞生长因子 信号转导子和转录激动子1 大鼠 Cerebral ischemia Behavior Training basic fibroblast growth factor Signal transducers and activators oftranscriptionl Rat
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