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1 μmol/L地塞米松处理48 h，建立胰岛素抵抗模型。用10 μmol/L的罗格列酮（阳性对照）和25、50、100 μmol/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、100 μmol/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 1 μmol/L dexamethasone for 48 h to establish an insulin resistance model. The insulin-resistant cells were treated with 10 μmol/L rosiglitazone (positive control) and 25, 50 or 100 μmol/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 100 μmol/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.

江苏省自然科学基金项目（BK20201480）