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人参皂苷F2通过PI3K/Akt途径改善3T3-L1脂肪细胞胰岛素抵抗 被引量:6

Ginsenoside F2 Improves Insulin Resistant in 3T3-L1 Adipocytes via the PI3K/Akt Signaling Pathway
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摘要 该研究探讨了人参皂苷F2对3T3-L1脂肪细胞胰岛素抵抗的影响及其机制。将3T3-L1前脂肪细胞诱导分化成熟后,用1μmol/L地塞米松处理48 h,建立胰岛素抵抗模型。用10μmol/L的罗格列酮(阳性对照)和25、50、100μmol/L人参皂苷F2处理胰岛素抵抗细胞12 h,检测细胞对2-NBDG的摄取。实验结束后用RT-qPCR检测各组细胞中葡萄糖转运蛋白4(GLUT-4)和胰岛素底物受体1(IRS-1)mRNA相对表达量,并利用Western blot检测PI3K/Akt信号通路中蛋白表达及其磷酸化水平。结果表明:与模型组相比,25、50、100μmol/L人参皂苷F2均能促进胰岛素抵抗3T3-L1脂肪细胞对2-NBDG的摄取,分别增加了12.58%、29.07%和34.62%(p<0.05);人参皂苷F2作用12 h后,GLUT-4和IRS-1 mRNA相对表达量以及PI3K、Akt的磷酸化水平显著提高(p<0.01)。该研究表明人参皂苷F2可通过促进胰岛素抵抗3T3-L1脂肪细胞中GLUT-4和IRS-1mRNA相对表达,增加PI3K和Akt蛋白磷酸化,从而激活PI3K/Akt信号通路,改善其糖代谢和胰岛素抵抗。 In this study,the effect of ginsenoside F2(GF2)on insulin resistance in 3T3-L1 adipocytes and the underlying mechanisms were investigated.After 3T3-L1 preadipocytes were induced to differentiate and mature,they were treated with 1μmol/L dexamethasone for 48 h to establish an insulin resistance model.The insulin-resistant cells were treated with 10μmol/L rosiglitazone(positive control)and 25,50 or 100μmol/L GF2 for 12 h,and the uptake of 2-NBDG by the cells was determined.After the experiments,real-time quantitative PCR was used to evaluate the relative mRNA expression levels of glucose transporter 4(GLUT-4)and insulin receptor substrate 1(IRS-1)in each group of cells.The protein expression and phosphorylation level of the PI3K/Akt signaling pathway were also evaluated by western blot.The results showed that compared with the model group,25,50,and 100μmol/L GF2 promoted the uptake of 2-NBDG in insulin-resistant 3T3-L1 adipocytes in a dose-dependent manner(increased by 12.58%,29.07%and 34.62%respectively;p<0.05).After the 12 h treatment with ginsenoside F2,the relative mRNA expression levels of GLUT-4 and IRS-1 as well as the phosphorylation levels of PI3K and Akt increased remarkably(p<0.01.This research shows that GF2 could activate the PI3K/Akt pathway,and improve glucose metabolism and insulin resistance,through promoting the relative mRNA expressions of GLUT-4 and IRS-1 in insulin-resistant 3T3-L1 adipocytes,and increasing the phosphorylation levels of PI3K and Akt proteins.
作者 韩胜强 谢元 李甫 胡烨烨 周静 胡卫成 张迹 HAN Shengqiang;XIE Yuan;LI Fu;HU Yeye;ZHOU Jing;HU Weicheng;ZHANG Ji(College of Food Science and Pharmacology,Xinjiang Agricultural University,Urumqi 830052,China;Jiangsu Collaborative Innovation Center of Regional Modern Agriculture&Environmental Protection,Huaiyin Normal University,Huaian 223300,China;Chengdu Institute of Biology,Chinese Academy of Sciences,Chengdu 610041,China)
出处 《现代食品科技》 CAS 北大核心 2022年第5期8-15,共8页 Modern Food Science and Technology
基金 江苏省自然科学基金项目(BK20201480)。
关键词 人参皂苷F2 3T3-L1脂肪细胞 PI3K/AKT信号通路 胰岛素抵抗 ginsenoside F2 3T3-L1 adipocytes PI3K/Akt pathway insulin resistance
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