检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:邢雪松[1] 吕威力[2] 曾亮[1] 王正东[1]
机构地区:[1]沈阳医学院,解剖学教研室,沈阳110034 [2]沈阳医学院,病理学教研室,沈阳110034
出 处:《解剖学杂志》2016年第6期660-663,共4页Chinese Journal of Anatomy
基 金:辽宁省科技厅科学技术计划资助项目(2013020216)
摘 要:目的:探讨穿梭箱训练对大鼠海马缺血后糖原合成酶激酶-3β(GSK-3β)表达及对神经干细胞增殖分化的影响机制。方法:采用大脑中动脉栓塞(MCAO)制作大鼠血管性痴呆模型,免疫组织化学检测穿梭箱训练后海马神经干细胞BrdU的表达,观察穿梭箱训练对血管性痴呆大鼠神经干细胞增殖分化的影响。检测缺血海马GSK3β的表达,观察穿梭箱训练对血管性痴呆大鼠GSK-3β的影响。结果:脑缺血再灌注第3天缺血海马神经元BrdU阳性细胞明显增多,第7天达高峰。GSK-3β反应产物脑缺血再灌注第7天较正常组增多,随缺血再灌注时间的进一步延长逐渐减少,第14天后持续低水平表达。穿梭箱训练后BrdU、GSK-3β蛋白的表达明显增加。结论:穿梭箱训练促进神经干细胞的增殖及缺血脑组织GSK-3β的表达,其作用可能由GSK-3β信号介导。Objective. To study the effect of behavior training on the expression of GSK-3β and hippocampal neurogenesis in a rat model of cerebral ischemia/reperfusion, and to explore the related molecular and behavior training mechanism. Methods: Behavior training was performed at day I after the ischemia/reperfusion. Middle cerebral artery occlusion (MCAO) was performed to establish the vascular dementia model. The expression of BrdU and GSK-3β in the hippocampus was detected with immtmohistochemical methods to explore the related neurogenesis and behavior training molecular mechanism. Results: BrdU positive cells in the hippocampus obviously increased at clay 3 and peaked at clay 7 of ischemia/reper/usion. GSK-3β reaction products increased gradually with the time of cerebral ischemia/reperfusion, reached the peak on day 7, and gradually decreased. After training, the expression of GSK-3β in hippocampous had apparently increased in each group. Conclusion: Behavior training promotes the expression of GSK-3β in the hippocampus tissues. These findings indicate that promotion of neural stem cell proliferation induced by behavior training may be mediated by GSK-3β signaling pathway.
关 键 词:行为学训练 糖原合成酶激酶-3B 神经干细胞 增殖 大脑中动脉栓塞 大鼠
分 类 号:R741[医药卫生—神经病学与精神病学]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.117