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机构地区:[1]沈阳医学院解剖学教研室,辽宁沈阳110034 [2]沈阳医学院病理学教研室,辽宁沈阳110034 [3]沈阳医学院信息技术中心计算机教研室,辽宁沈阳110034
出 处:《中风与神经疾病杂志》2015年第7期616-618,共3页Journal of Apoplexy and Nervous Diseases
基 金:辽宁省科技厅科学技术计划资助项目(No.2013020216)
摘 要:目的探讨不同干预方法对血管性痴呆大鼠神经再生及脑组织N-myc蛋白表达的影响。方法雄性Wistar大鼠实验随机分为4组:假手术组,模型组,训练组,b FGF组。采用两血管阻断加硝普钠降压法制作大鼠血管性痴呆(VD)动物模型,用HE、和免疫组织化学方法检测海马组织N-myc蛋白的表达及穿梭箱训练和b FGF的干预作用。结果随着脑缺血再灌注3 d缺血海马神经元N-myc阳性细胞明显增多,随缺血再灌注时间的延长逐渐增多,14 d达高峰。应用穿梭箱训练和b FGF的干预后N-myc阳性细胞明显增加。结论穿梭箱训练和b FGF促进神经再生及缺血脑组织N-myc蛋白的表达,提示穿梭箱训练和b FGF促进神经再生作用可能由N-myc信号介导。Objective To investigate the expression of N-myc expression and hippocampal neurogenesis in a rat model of cerebral ischemia/reperfusion, and to explore the related molecular and different interferences mechanism. Meth- ods Wistar rats were randomized into sham groups training groups,ischemia and reperfusion groups and bFGF group. Be- havior training was performed at day 1 after the ischemia and reperfusion. The model of middle cerebral arteries occlusion (MCAO) were performed with intraluminal filament blockade. The expression of N-myc and in the hippocampus was detec- ted with HE and immunohistochemical methods. Results Mter 3 days, N-myc positive cells in the hippocampus were obvi- ously increased. N-myc reaction products were increased gradually with the time of cerebral ischemia/reperfusion, reached the peak on day 14,and then gradually decreased. After training and bFGF intervening, the expression of hippocampal N- myc had apparently increased in each group. Conclusion Behavior training and bFGF promoted the expression of N-myc in the hippocampus tissues. These findings indicate that training and bFGF promotion of neural stem cell proliferation may be mediated by N-myc signaling pathway.
分 类 号:R749.13[医药卫生—神经病学与精神病学]
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