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。
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.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
2005年第6期708-711,共4页
Acta Academiae Medicinae Sinicae
基金
国家自然科学基金(30400171
30370560
30430270)
国家重点基础性研究项目(973项目)(2006CB500703)~~
