芒果苷对HepG2细胞胰岛素抵抗的影响

目的探讨芒果苷在体外的降糖效果及对胰岛素传导关键信号蛋白磷酸化蛋白激酶Bp-AKT(Thr308)]、磷酸化糖原合成激酶3βp-GSK-3β(Ser9)]、腺苷酸活化蛋白激酶(AMPKα)、葡萄糖转运蛋白2(GLUT2)表达的影响。方法培养HepG2细胞,用CCK-8法检测芒果苷对HepG2细胞增殖的影响;采用浓度为1×10^-6 mol/L的胰岛素刺激细胞36 h建立胰岛素抵抗模型;用葡萄糖检测试剂盒检测芒果苷对胰岛素抵抗HepG2细胞葡萄糖消耗的影响,用western blot法探讨其可能的作用机制。结果芒果苷浓度在>125μg/mL浓度后对HepG2细胞生长有抑制作用,故采用浓度为60、30、15μg/mL的芒果苷进行葡萄糖消耗实验,发现实验组与模型组比较,葡萄糖消耗量明显增加且具有显著性差异(P<0.01,P<0.05)。western blot结果表明,与正常组比较,模型组p-AKT(Thr308)、p-GSK-3β(Ser9)、AMPKα、GLUT2蛋白表达明显降低且存在显著性差异(P<0.05);与模型组比较,实验组蛋白表达均明显增加,且高剂量组均存在显著性差异(P<0.01,P<0.05),低剂量组除GLUT2蛋白表达具有显著性差异(P<0.05),其他蛋白虽有增加但无统计学意义。结论芒果苷对HepG2细胞胰岛素抵抗有改善作用,其作用机制可能是通过调控p-AKT(Thr308)、p-GSK-3β(Ser9)、AMPKα及GLUT2等蛋白的表达来改善2型糖尿病的胰岛素抵抗。

Effect of Mangiferin on Insulin Resistance in HepG2 Cells

Objective The hypoglycemic effect of mangiferin in vitro and the effect of mangiferin on the expression of insulin key signal proteins Phospho-protein kinase Bp-AKT(Thr308)],Phospho-glycogen synthase kinase 3βp-GSK-3β(Ser9)],(AMP)-activated protein kinaseαand Glucose Transporter 2(GLUT2).Methods HepG2 cells were cultured and the effect of mangiferin on HepG2 cells proliferation was determined by CCK-8 method.The insulin resistance model was established by stimulating cells with a concentration of 1×10^-6 mol/L for 36 hours.The glucose test kit was used to detect the effect of mangiferin on glucose depletion in insulin-resistant HepG2 cells,and the possible mechanism of mangiferin was discussed by western blot assay.Results The concentration of mangiferin inhibited the growth of HepG2 cells at a concentration greater than 125μg/mL.The final concentration was 60,30,15μg/mL for glucose consumption experiments.It was found that the glucose consumption of the experimental groups was significantly increased compared with the model group(P<0.01,P<0.05).Western blot analysis showed that compared with the normal group,the expression of p-AKT(Thr308),p-GSK-3β(Ser9),AMPKα,GLUT2 protein in the model group was significantly decreased(P<0.05).Compared with the model group,the expression of experimental groups was significantly increased,and there was significant difference in the high-dose group(P<0.01,P<0.05).There was a significant difference in the expression of GLUT2 protein in the low-dose group(P<0.05),although other proteins increased,not statistically significant.Conclusion Mangiferin can improve insulin resistance in HepG2 cells,and its mechanism may be to improve insulin resistance in type 2 diabetes by regulating the expression of p-AKT(Thr308),p-GSK-3β(Ser9),AMPKαand GLUT2 proteins.