桑叶提取物对胰岛素抵抗HepG2细胞葡萄糖摄取的影响及其分子机制
Effect of mulberry leaves extracts on glucose uptake of insulin-resistant HepG2 cells and the mechanism
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摘要:
本文研究了桑叶多糖 (mulberry leaves polysaccharides, MLP)、桑叶黄酮 (mulberry leaves flavonoids, MLF) 和桑叶水提物 (mulberry leaves hot water extracts, MLE) 对胰岛素抵抗状态下HepG2 (IR-HepG2) 细胞葡萄糖摄取的影响, 并探讨其分子机制。采用高浓度胰岛素 (INS) 持续作用于HepG2细胞24 h建立胰岛素抵抗模型, 加一定剂量的MLP、MLF和MLE干预, 添加或不添加胰岛素刺激, 测定各组细胞的葡萄糖消耗量。Western blotting法检测磷酸化腺苷酸活化蛋白激酶 (AMPK) 磷酸化水平及胰岛素信号通道PI3K关键酶蛋白激酶B (Akt) 磷酸化水平。结果表明: MLP、MLF和MLE明显增加了细胞的葡萄糖消耗; MLE能明显提高IR-HepG2细胞AMPK磷酸化水平; MLP、MLF和MLE对Akt磷酸化没有影响, 可以明显改善胰岛素抵抗状态下HepG2细胞对葡萄糖的利用, MLE的降糖作用机制可能与胰岛素无关, 是通过AMPK通道促进葡萄糖的吸收而实现的。
Abstract:The effect and mechanism of mulberry leaves extracts (MLE) on glucose uptake of insulin- resistant HepG2 cells in vitro was explored. The insulin resistant models of HepG2 were induced by high concentration of insulin for 24 h. The models were incubated in a buffer containing mulberry leaves extracts. The glucose consumption was detected by glucose assay kits and the AMP-activated protein kinase (AMPK), Akt activation was examined by Western blotting. Mulberry leaves polysaccharides, mulberry leaves flavonoids and mulberry leaves extracts advanced glucose uptake of insulin-resistant HepG2 cells; Mulberry leaves extracts enhance phosphorylation of AMPK. Mulberry leaves extracts do not change the phosphorylation status of Akt. The glucose consumptions of insulin resistant model of HepG2 were promoted by mulberry leaves extracts. MLE stimulates HepG2 cell AMPK activity acutely without changing the Akt activity.
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