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本研究旨在探讨海马内不同亚型雌激素受体α(estrogen receptorα,ERα)及相关信号分子与糖尿病引起的空间认知障碍的相关性。腹腔注射四氧嘧啶建立1型糖尿病小鼠模型,并采用Morris水迷宫方法检测模型组小鼠是否存在空间认知障碍;然后用Western blot比较模型组和正常对照组小鼠海马内ERα不同亚型ER-α36和ER-α66的表达,同时检测窖蛋白-1(caveolin-1)、PKCα、cAMP反应元件结合蛋白2(cAMP-response element binding protein 2,CREB2)和突触素(synaptophysin,Syn)的表达变化。结果显示,相对对照组,糖尿病模型组小鼠空间训练第3天和第5天的逃避潜伏期显著延长(P<0.05),撤去平台后游泳路程增加;模型组小鼠海马caveolin-1、PKCα表达量显著降低(P<0.05),ER-α66蛋白表达水平没有明显变化,而ER-α36和CREB2的表达量显著升高(P<0.05)。以上结果提示,海马内ER-α36及相关信号分子的异常表达对糖尿病小鼠空间认知障碍形成可能具有重要的作用。
This study aimed to investigate the relationship between estrogen receptor alpha (ERα) and related signaling molecules in different subtypes of hippocampus and spatial cognitive impairment caused by diabetes mellitus. The model of type 1 diabetic mice was established by intraperitoneal injection of alloxan and the spatial cognitive impairment was detected by Morris water maze. Then the expression of ERα in the hippocampus was compared between the model group and the normal control group ER36, ER-α36 and ER-α66, and to detect the expressions of caveolin-1, PKCα, cAMP-response element binding protein 2 (CREB2) and synaptophysin (Syn) Changes in expression. The results showed that compared with the control group, the escape latency of the mice in the diabetes model group was significantly prolonged on days 3 and 5 (P <0.05), and the swimming distance was increased after the platform was removed. The expression of caveolin-1 and PKCα (P <0.05). The expression of ER-α66 protein did not change significantly, while the expression of ER-α36 and CREB2 was significantly increased (P <0.05). The above results suggest that the abnormal expression of ER-α36 and related signal molecules in hippocampus may play an important role in the formation of spatial cognitive impairment in diabetic mice.