【摘要】 目的探讨胰岛素对高糖培养海马神经元的保护作用及其作用机制。方法选择新生24h SD大鼠,取海马神经元进行原代培养,分为正常对照组(NC组),高糖模型组(HG组),实验组(RI组),采用Tunel检测海马神经元的凋亡,Western blot法检测各组P-IRS、IRS1、P-AKT、AKT、Bcl-2、Bax蛋白的表达。结果与NC组相比,HG组海马神经元凋亡率显著增加(P<0.01);与HG组相比,RI组凋亡率显著降低(P<0.01)。与NC组相比,HG组P-IRS、IRS1蛋白表达显著降低(P<0.05);RI组P-IRS表达及P-IRS/IRS1显著升高(P<0.01)。与HG组相比,RI组P-IRS表达及P-IRS/IRS1显著升高(P<0.01)。与NC组相比,HG组AKT表达显著降低(P<0.01);RI组P-AKT、AKT表达及P-AKT/AKT显著升高(P<0.01)。与HG组相比,RI组P-AKT、AKT表达及P-AKT/AKT显著升高(P<0.01)。与NC组相比,HG组Bcl-2、Bcl-2/Bax蛋白表达显著降低(P<0.01);RI组Bcl-2、Bcl-2/Bax蛋白表达显著升高(P<0.01),Bax蛋白表达显著降低(P<0.01)。与HG组相比,RI组Bcl-2、Bcl-2/Bax蛋白表达显著升高(P<0.01),bax蛋白表达显著降低(P<0.01)。结论胰岛素能够抑制高糖培养海马神经元的凋亡,其作用可能是通过活化IRS1/PI3K/AKT信号通路,同时上调Bcl-2/Bax实现的。更多还原

【Abstract】 Objective To explore the protective effect and mechanism of insulin on hippocampal neurons cultured in high glucose.Methods Hippocampus were obtained from newborn 24 h SD rats and then Primary cultured.According to the purpose of the study,hippocampal neurons were divided into 3 groups: normal control group(NC group),high glucose group(HG group),experimental group(RI group).We detected the apoptosis of neurons with TUNEL.And the expression of P-IRS,IRS1,P-AKT,AKT,Bcl-2 and Bax was detected by using western blot.Results Compared with the NC group,the apoptosis rate of hippocampal neurons in HG group was increased significantly(P < 0.01).Compared with the HG group,the apoptosis rate of hippocampal neurons in RI group was decreased significantly(P < 0.01).Compared with the NC group,the expression of P-IRS and IRS1 of HG group was decreased significantly(P <0.05),the expression of P-IRS and P-IRS/IRS1 of RI group was increased significantly(P < 0.01).Compared with the HG group,the expression of P-IRS and P-IRS/IRS1 of RI group was increased significantly(P < 0.01).Compared with the NC group,the expression of AKT of HG group was decreased significantly(P < 0.01),the expression of P-AKT,AKT and P-AKT/AKT of RI group was increased significantly(P < 0.01).Compared with the HG group,the expression of P-AKT,AKT and P-AKT/AKT of RI group was increased significantly(P < 0.01).Compared with the NC group,the expression of Bcl-2 and Bcl-2/Bax of HG group was decreased significantly(P < 0.01),the expression of Bcl-2 and Bcl-2/Bax of RI group was increased significantly(P < 0.01),and the expression of bax was decreased significantly(P < 0.01).Compared with the HG group,the expression of Bcl-2 and Bcl-2/Bax of RI group was increased significantly(P < 0.01),and the expression of bax was decreased significantly(P < 0.01).Conclusion Insulin could reduce the apoptosis of neurons which cultured in high glucose by activating the IRS1/PI3K/AKT signal pathway and up-regulating Bcl-2/Bax.更多还原