【摘要】 目的探讨糖尿病大鼠皮层神经元β淀粉样蛋白(Aβ)以及谷氨酸转运体的功能变化及其可能机制。方法用链脲佐菌素建立糖尿病大鼠模型,并检测正常对照组、糖尿病(DM)模型组、DM+NaCl组、DM+LiCl组糖原合酶激酶-3(GSK-3)的活性、谷氨酸转运体功能及Aβ水平。结果DM组与对照组相比,GSK-3活性(P<0.05)和Aβ40生成(P<0.01)显著增加,谷氨酸转运体的功能显著减弱(P<0.05);GSK-3的抑制剂LiCl能显著降低糖尿病鼠Aβ40水平(P<0.01)和改善谷氨酸转运体的功能(P<0.05)。结论糖尿病大鼠皮层Aβ40生成增加、谷氨酸转运体的功能降低、GSK-3升高在这一病理改变过程中起着重要作用。更多还原

【Abstract】 Objective To investigate the alteration of β-amyloid (Aβ) and glutamate transporter in the brain cortex of diabetes mellitus (DM) rats and the underlying mechanism. Methods The rats were randomly divided into control, DM, DM+NaCl, and DM+LiCl groups and diabetes was induced by streptozotocin. The activity of glycogen synthase kinase-3(GSK-3)and the function of glutamate transporter were measured by 32P-labelling. The amount of Aβ was determined by enzyme-linked immunosorbentassay. Results In DM group, the level of Aβ40 increased(P < 0.01), but the function of glutamate transporter was impaired(P < 0.05). The activity of GSK-3 was stimulated(P < 0.05). Compared with DM group, the level of Aβ40 was restored(P < 0.01), and the function of glutamate transporter was enhanced(P < 0.05) in LiCl treated group, accompanied by a decreased activity of GSK-3. Conclusion Overproduction of Aβ and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a curial role in this process.更多还原