| 干预GLP-1通路保护过氧化氢诱导心肌细胞凋亡的研究 |
| 投稿时间：2016-07-11 修订日期：2016-07-28 点此下载全文 |
| 引用本文：赵树梅,张谦,郭春艳.干预GLP-1通路保护过氧化氢诱导心肌细胞凋亡的研究[J].医学研究杂志,2017,46(3):98-101 |
| DOI：
10.11969/j.issn.1673-548X.2017.03.025 |
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| 基金项目:首都医科大学基础-临床科研基金资助项目（13-JL58） |
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| 中文摘要:目的 观察Exendin-4（Ex-4，GLP-1受体激动剂）对H2O2孵育的心肌细胞凋亡的影响，探讨GLP-1通路干预心肌细胞损伤的机制。方法 分离、培养心室肌细胞，分成5组∶A组为对照组；B组为H2O2干预组（100μmol/L，24h）；C组为H2O2+Ex-4（Ex-10nmol/L，孵育24h）组；D组为H2O2+Ex-4（Ex-20nmol/L，孵育24h）组；E组为H2O2+Ex-4+LY294002（Ex-20nmol/L，LY-5μmol/L，孵育24h）组。荧光染色测定各组细胞内活性氧簇（ROS）生成的水平；流式细胞仪测定各组细胞凋亡率情况。以Western blot法测定各组细胞凋亡蛋白及机制蛋白（PI3K/AKT）的表达。结果 与H2O2孵育组相比，Ex-4干预使得心肌细胞内ROS水平下降，细胞凋亡率下降，在高剂量组（D组）均达到差异统计学意义（P<0.05）。同时，Ex-4干预可使p-AKT/AKT表达显著增加，caspase-3表达显著下降（P<0.05）；而这些效应可被LY294002共孵育（E组）所逆转。结论 干预GLP-1通路，可缓解H2O2诱导的心肌细胞凋亡，此效应至少部分是通过影响PI3K/AKT途径实现的。 |
| 中文关键词:GLP-1通路 氧化应激 心肌细胞凋亡 PI3K/AKT |
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| Improvement of Cardiomyocyte Apoptosis Induced by Hydrogen Peroxide via the Intervention of GLP-1 Signal Pathway |
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| Abstract:Objective To observe the effect of Exendin-4 on the apoptosis of cardiomyocyte induced by H2O2, and approach the relationship between GLP-1 signal pathway and the injury of cardiomyocyte. Methods Cardiomyocytes were isolated and cultured, and were divided into 5 groups. Intercelluar ROS (reactive oxygen species) was measured, and cell apoptosis rate was evaluated by Flow cytometry in different groups. Also expressions of apoptosis-associated proteins (caspase-3) and PI3K/AKT were evaluated by western blot. Results Compared with H2O2 group, Ex-4 co-incubation decreased the production of intercelluar ROS levels, also improved the cardiomyocyte apoptosis. At the same time, Ex-4 resulted in the alterations in expressions of the caspase-3 and p-AKT/AKT proteins. However, these effects of Exendin-4 were counteracted significantly by the co-incubation of LY294002. Conclusion The interventions of GLP-1 signal pathway can improve cardiomyocyte apoptosis induced by H2O2 incubation, and the mechanisms might partly attribute to the PI3K/AKT system. |
| keywords:GLP-1 signal pathway Oxidative stress Cardiomyocyte apoptosis PI3K/AKT |
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