【摘要】 目的:探讨胰高血糖素样肽1(GLP-1)对APP瑞典突变体质粒转染构建的阿尔茨海默病(AD)细胞模型的保护作用及可能机制。方法:将人肾上皮细胞系HEK293分为对照组、转染组、GLP-1干预组,对照组不予任何处理,其他两组构建APP瑞典突变体质粒转染的AD细胞模型,GLP-1干预组分别加入不同浓度(5、10、20、50、100μmol/L)的GLP-1;3组均在培养前及培养6、12、24、48及72 h收集细胞上清液,ELISA检测β淀粉蛋白(Aβ)含量,QDs-SA细胞免疫荧光染色检测Aβ的变化,运用DCFH-DA检测细胞内活性氧(ROS)。结果:与对照组比较,转染组Aβ含量及ROS水平明显升高(P<0.05);GLP-1干预组不同浓度的GLP-1和培养时间增加均能减少Aβ含量和ROS水平。结论:APP瑞典突变体质粒转染的AD细胞模型会使Aβ含量明显升高,产生氧化应激损伤,GLP-1能通过降低氧化应激损伤减少细胞内Aβ聚集,并具有浓度-时间依赖性。更多还原

【Abstract】 Objective: To study the protective effects of glucagon-like peptide 1(GLP-1) on Alzheimer’s disease(AD) cell model constructed by transfecting APP Swedish mutant plasmid.Methods: HEK293 cells were divided into control group,transfection group and GLP-1 groups.The control group didn’t accept any treatment,and the other groups were transfected with APP Swedish mutant plasmid to construct AD cell model.GLP-1 groups were treated with different doses(5,10,20,50,100 μmol/L) of GLP-1 respectively.β-amyloid(Aβ) content was measured with ELISA and QDs-SA immunofluorescence staining,and ROS level was detected with DCFH-DA.Results: Aβ level and ROS level were higher in AD cell groups than those in control group(P<0.05).GLP-1 at different concentrations,and with the increase of culture time could reduce Aβ contents and ROS levels.Conclusions: Transfecting AD cell model with APP Swedish mutant plasmid leads to increase of Aβ level and oxidative stress injury.GLP-1 can decrease Aβ accumulation in dose and time dependent manner by reducing oxidative stress injury.更多还原