中文摘要：

目的探讨瘦素（1eptin）与阿尔茨海默病的联系。方法将人神经纤维母细胞瘤细胞系（SH—SY5Y）分为3组：对照组、冈田酸（okadaic acid，OA）损伤模型组（40nmol／LOA诱导12h）和Leptin处理组。用OA诱导SH—SY5Y，建立阿尔茨海默病细胞模型。Leptin处理组是在模型组基础上，给予外源性leptin（0．4仙g／m1）处理6h，用WesternBlot检测细胞周期依赖性蛋白激酶5（Cdk5）和β-actin蛋白表达水平。瘦素受体（ObR）和Cdk5的共定位情况用双重免疫荧光染色检测。结果模型诱导成功后，Westel33 Blot显示Cdk5表达明显升高（p〈0．01）；给予leptin后，Cdk5蛋白表达显著降低（p〈0．01）。双染法免疫荧光实验表明，SH—SY5Y细胞中ObR和Cdk5蛋白均主要在细胞质中表达，并且红色和绿色标记重叠为橙色荧光，可认为两种蛋白共定位，提示ObR和Cdk5之间可能存在相互作用。结论Leptin能够在体外降低阿尔茨海默病相关的Cdk5表达，为其治疗提供了新靶点。

英文摘要：

Abstract： Objective To study the association between leptin and Alzheimer＇s disease （AD）. Methods SH-SY5Y cells were randomly divided into control group, Okadaic acid （OA） injury model group, and leptin treatment group. An AD model was established by inducing SH-SY5Y with 40nmol/L OA. Leptin treatment group was treated with 0.4μg/ml exogenous leptin for 6 h. Expression levels of cell cycle-dependent Cdk5 and β -actin proteins were measured by Western blot. ObR and Cdk5 co- localization was detected by dual immunofluorescent staining assay. Results Western blot showed that the Cdk5 expression level was significantly higher after the model was established （P 〈 0.01） and significantly lower after leptin was given （P 〈 0.01）. Double immunofluorescence staining assay showed that the ObR and Cdk5 proteins were expressed mainly in cytoplasm of SH-SY5Y ceils. The red and green markers were overlapped into orange fluorescence, which could be considered as the co-localization of the two proteins, suggesting that ObR interacts with Cdk5. Conclusion Leptin can down-regulate Alzheimer＇s disease-related Cdk5 exoression in vitro, thus providing a new target for the treatment of Alzheimer＇s disease.