中文摘要：

研究了罗格列酮对链脲佐菌素（streptozotocin, STZ）脑室内注射的阿尔茨海默病（AD）模型小鼠学习记忆减退的影响及机制．在小鼠脑室内注射STZ建立AD模型，治疗组小鼠采用罗格列酮灌胃给药30天．Morris水迷宫实验检测小鼠学习记忆能力，免疫印迹和免疫荧光检测Tau蛋白的磷酸化、神经丝（NFs）蛋白的磷酸化及糖基化、JNK和ERK蛋白的表达，微管结合实验检测Tau蛋白与微管的组装功能，荧光染料Fluoro-Jade B检测小鼠脑内退变神经元．结果显示，相比对照组，模型组小鼠平均逃避潜伏期和路径长度明显增加、穿越隐匿平台次数明显减少、Tau和NFs蛋白表达过度磷酸化、NFs蛋白糖基化减弱，而用罗格列酮干预的小鼠学习记忆改善并且Tau和NFs蛋白的磷酸化水平降低、NFs蛋白糖基化水平增加，Tau蛋白与微管结合能力改善，模型组JNK的磷酸化高于对照组和治疗组、模型组ERK1的磷酸化低于对照组和治疗组、各组在ERK2磷酸化无明显差异，模型组小鼠脑中FJB标记的退化神经元明显多于对照组和治疗组．结果说明，罗格列酮能改善STZ脑室内注射引起的小鼠学习记忆减退，其机制可能与改善胰岛素信号通路、降低Tau和NFs蛋白的过度磷酸化、减少神经退行性变有关．

英文摘要：

Research on the protective effect and mechanism of rosiglitazone on learning and memory impairment of AD-like mice induced by streptozotocin （STZ） intracerebroventricular （i.c.v.） injection. STZ i.c.v. injection was used to establish AD mice model and the treatment mice were administered orally with rosiglitazone for 30 days. Morris water maze was applied to detect the learning and memory ability of mice and Western blot and immunofluorescence to analyze the phosphorylation levels of Tau,the expression levels of phosphorylation and glycosylation of neurofilaments （NFs） protein, the expression levels of JNK and ERK. The microtubule binding assay was used to detect the assembly function of Tau binding with microtubule. The degenerative neurons were labeled by Fluoro -Jade B （FJB）. Compared with the control group, the escape latency and path length were increased of the model group with less number of crossing hidden platform, and the Tau and NFs proteins were hyperphosphorylated and the glycosylation of NFs protein were lower. But compared with the model group, the rosiglitazone significantly improved the learning and memory ability of mice and decreased the hyperphosphorylated levels of Tau and NFs proteins, increased the glycosylation of NFs protein, and increased the microtubule-binding of Tau in treated-mice. The phosphorylated expression levels of JNK of model group were higher than the other two groups, while ERK1 were lower, but there was no significant difference of ERK2 in three groups. And the numbers of FJB-degenerative neurons of model group were much more than the other two groups. Rosiglitazone could protect learning and memory impairment of AD-like mice induced by STZ i.c.v. injection, which may be related to ameliorate the insulin signal pathway, decrease the hyperphosphorylation of Tau and NFs proteins, and protect from the neural degeneration.