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明日叶查尔酮对胰岛素抵抗细胞PI3K-Akt-GLUT4信号通路的影响

发布时间:2019-07-22 08:20
【摘要】:目的研究明日叶查尔酮(Angelica keiskei chalcones,AC)对胰岛素抵抗L6细胞磷脂酰肌醇3激酶-蛋白激酶-葡萄糖转运体4(PI3K-Akt-GLUT4)信号通路的影响。方法采用高浓度胰岛素诱导的胰岛素抵抗L6细胞,分别加入5、10、20μmol/L终浓度的明日叶查尔酮共同培养24 h,葡萄糖氧化酶法测定细胞上清液中葡萄糖含量,逆转录聚合酶链式反应方法检测细胞PI3K和Akt的mRNA表达水平,蛋白印迹法检测GLUT4和Akt的蛋白表达水平。结果胰岛素抵抗组细胞培养液的葡萄糖含量显著高于空白对照组(P0.05),而PI3K mRNA、Akt mRNA和GLUT4、Akt蛋白表达水平则降低(P0.05);中、高剂量AC组细胞培养液葡萄糖含量均低于胰岛素抵抗组(P0.05),而PI3K mRNA、Akt mRNA和GLUT4、Akt蛋白表达水平则升高(P0.05)。结论明日叶查尔酮可上调L6细胞胰岛素抵抗模型PI3K-AktGLUT4信号通路的表达水平,增强其对葡萄糖的摄取利用,改善胰岛素抵抗。
[Abstract]:Aim to study the effect of tomorrow Chalcone (Angelica keiskei chalcones,AC on phosphatidylinositol 3 kinase protein kinase glucose transporter 4 (PI3K-Akt-GLUT4) signaling pathway in insulin resistant L6 cells. Methods High concentration insulin induced insulin resistant L6 cells were co-cultured with 5 渭 mol / L, 10 渭 mol / L and 20 渭 mol / L tomorrow for 24 H. the glucose content in the culture medium was determined by glucose oxidase method, the mRNA expression of PI3K and Akt was detected by reverse transcriptase polymerase chain reaction (RT-PCR), and the protein expression of GLUT4 and Akt was detected by Western imprinting. Results the glucose content in the cell culture medium of insulin resistance group was significantly higher than that of blank control group (P 0.05), while the expression of PI3K mRNA,Akt mRNA and GLUT4,Akt protein was decreased (P 0.05). The glucose content of high dose AC group was lower than that of insulin resistance group (P 0.05), while the expression level of PI3K mRNA,Akt mRNA and GLUT4,Akt protein was increased (P 0.05). Conclusion tomorrow leaf chalcone can up-regulate the expression of PI3K-AktGLUT4 signaling pathway in L6 cells with insulin resistance, enhance its uptake and utilization of glucose, and improve insulin resistance.
【作者单位】: 厦门大学公共卫生学院;中国人民解放军总医院;
【基金】:福建省自然科学基金计划资助项目(No.2014J05098)
【分类号】:R96

【参考文献】

相关期刊论文 前5条

1 张茁;孙文;刘铜华;郭璇;候丹;许光远;吴丽丽;秦灵灵;侯毅;张露;张程斐;;山柰酚对2型糖尿病小鼠骨骼肌PI3K-AKT-GLUT4信号通路的影响[J];世界科学技术-中医药现代化;2016年07期

2 周雪梅;田春雨;喇孝瑾;陈国林;张碧n,

本文编号:2517490


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