| 胰岛素对高糖培养海马神经元凋亡及IRS/PI3K/AKT信号通路、Bcl-2与Bax蛋白表达的影响 |
| 投稿时间：2016-09-20 修订日期：2016-09-29 点此下载全文 |
| 引用本文：张元浩,闫斌,王靖博,田国庆,张宏,刘玉琴.胰岛素对高糖培养海马神经元凋亡及IRS/PI3K/AKT信号通路、Bcl-2与Bax蛋白表达的影响[J].医学研究杂志,2017,46(3):60-65 |
| DOI：
10.11969/j.issn.1673-548X.2017.03.016 |
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| 基金项目:北京市中医药科技发展基金资助项目（JJ2015-68） |
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| 中文摘要: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。 |
| 中文关键词:胰岛素 高糖 海马神经元 凋亡 作用机制 |
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| Effects of Insulin on the IRS/PI3K/AKT Signal Pathway, Bcl-2 and Bax Expression and the Apoptosis of Hippocampal Neurons Culturedin High Glucose |
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| Abstract:Objective To explore the protective effect and mechanism of insulin on hippocampal neurons cultured in high glucose. Methods Hippocampus were obtained from newborn 24h 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. |
| keywords:Insulin High glucose Hippocampal neurons Apoptosis Mechanism |
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