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作 者:郭灵[1] 崔卫刚[1] 蓝玲[1] 邓祥发[1] 曾庆堂[1] 林丹[1] 磨洁琳[1]
机构地区:[1]广西医科大学人体解剖学教研室,广西南宁530021
出 处:《解剖学研究》2009年第2期99-102,共4页Anatomy Research
基 金:广西科学基金(桂科自0542069)
摘 要:目的揭示1型糖尿病继发性脑病变(糖尿病脑病)的发生与海马齿状回颗粒下区(SGZ)神经干细胞增殖之间的关系。方法应用链脲佐菌素(溶解于柠檬酸缓冲液中)腹腔注射,将成年雄性Wistar大鼠建立成1型糖尿病脑病模型;将用柠檬酸缓冲液腹腔注射的大鼠或正常大鼠分别作为载体模型组或正常对照组。在建立模型成功后的60d,用Morris水迷宫和5-溴脱氧尿嘧啶(BrdU,一种神经干细胞合成DNA的标记物)免疫组化方法,观察各组大鼠空间学习记忆能力以及SGZ神经干细胞(BrdU阳性细胞)的变化。结果1型糖尿病脑病模型大鼠的逃避潜伏期和游泳距离均较载体模型组或正常对照组大鼠明显延长(P<0.01);而且该脑病组大鼠SGZ的BrdU阳性细胞数也明显低于载体模型组或正常对照组大鼠(P<0.01)。结论个体内长期缺乏胰岛素可导致SGZ神经干细胞增殖出现障碍,从而引发空间学习记忆能力下降,这可能是诱发1型糖尿病脑病的一个因素。Objective To examine the changes in the spatial learning and memory, and in the proliferation of neural stem cells in the hippocampal dentate gyrus of streptozotocin-induced type 1 diabetic encephalopathy rats. Methods Adult male Wistar rats were randomly divided into three groups: diabetic encephalopathy, vehicle control and intact control. The diabetic eneephalopathy model was indued by a dosage of intraperitoneal injection of streptozotocin. After 60 clays of developing the models, Morris water maze and bromodeoxyuridine (BrdU) immunohistochemistry were administered to detect the changes in spatial learning and memory as well as in the proliferation of neural stem cells (BrdU-immunoreactive cells, BrdU-IR cells)in the subgranular zone (SGZ)of each rat. Results Both escape latency and swimming distance of diabetic encephalopathy rats were significantly extended in comparison of those in vehicle control or intact control rats (P〈O.01). Furthermore, the number of BrdU-IR cells in SGZ of diabetic encephalopathy rats was also significantly smaller than that of vehicle or intact control rats (P〈 0.01 ). Conclusion Long-termed lack of insulin in the rats with type 1 diabetes can intervene the proliferation of neural stem cells in SGZ, which may result in disorders in spatial learning and memory. The above data indicate that impairments in proliferation of neural stem cells in adult hippocampal dentate gyrus may be one factor inducing type 1 diabetic encephalopathy.
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