金线莲苷促进骨骼肌细胞摄取葡萄糖的分子机制研究

Molecular Mechanism of Kinsenoside in Promoting Glucose Uptake in Skeletal Muscle Cells

在本研究中,先诱导大鼠骨骼肌细胞分化为成熟的肌管细胞,然后以肌管细胞为模型,在胰岛素敏感和胰岛素抵抗的情况下,通过蛋白免疫印迹的方法检测金线莲苷对蛋白激酶Akt和AMPK的活化,以荧光标记的2-脱氧葡萄糖为能量底物检测金线莲苷处理前后细胞对葡萄糖的摄取。结果显示在正常细胞中,10 nM金线莲苷作用24 h可显著增加Akt(34.53%,p<0.05)和AMPK的活性(149.92%,p<0.05),同时促进细胞对葡萄糖的摄取(43.35%,p<0.05)。在胰岛素抵抗的细胞中,金线莲苷对AMPK的活化不受影响,并且可改善胰岛素对Akt的激活作用(79.05%,p<0.05)。在正常及胰岛素抵抗的情况下,金线莲苷对胰岛素诱导的葡萄糖摄取都具有协同作用。这些结果表明金线莲苷可通过调控Akt和AMPK的活性改善细胞胰岛素抵抗,促进胰岛素抵抗细胞对葡萄糖的摄取。

In this study, rat skeletal muscle myoblasts were induced to differentiate into mature myotubes. The effect of kinsenoside on the Akt and AMPK activation was examined by western blot and glucose uptake was measured by fluorescence-labeled 2-deoxyglucose in both insulin-sensitive and insulin-resistant myotubes. The results showed that in normal cells, treatment with 10 nM kinsenoside for 24 h increased the activity of Akt（34.53%, p〈0.05） and AMPK（149.92%, p〈0.05）, and simultaneously promoted cellular uptake of glucose effectively（43.35%, p〈0.05）. In insulin resistant cells, the impaired insulin-stimulated Akt activation was ameliorated（79.05%, p〈0.05） by kinsenoside treatment. In the case of insulin sensitive and insulin resistant state, kinsenoside exhibited synergistic effect on the insulin-induced glucose uptake. These results suggested that kinsenoside might overcome insulin resistance via modulating both Akt and AMPK activity, leading to increase glucose uptake in insulin resistant cells.