芒果苷对L6细胞葡萄糖消耗的影响及其作用机制研究

目的观察芒果苷对L6细胞葡萄糖消耗的影响,并探讨其分子机制。方法以芒果苷干预L6肌管细胞,葡萄糖氧化酶法检测葡萄糖消耗量,western-blot方法检测葡萄糖转运蛋白4(GLUT4)的表达量及其急性转位作用,免疫共沉淀(IP)联合western-blot方法检测AKT激酶活性。结果芒果苷处理可激活L6细胞的AKT激酶(与对照组比,P=0.001),提高L6细胞的葡萄糖消耗(P=0.011或P=0.000)且呈剂量-反应关系(P=0.000),上调GLUT4的蛋白表达量(P=0.001或P=0.000)并促进GLUT4在细胞内发生急性转位(P=0.005,P=0.001或P=0.026),使该蛋白由胞浆经细胞骨架转位至细胞膜。结论芒果苷可促进L6细胞的葡萄糖消耗量,调节GLUT4的表达及其在细胞内的急性转位,激活AKT激酶活性,因此,芒果苷具有潜在的辅助降血糖作用。

The effect of mangiferin on glucose consumption of L6 cell and the study of its molecular mechanism

Objective molecular mechanism. To observe the effect of mangiferin on glucose consumption of L6 cell, and to analyze its Methods The differentiated myoblast cells were intervened with mangiferin, then the glucose consumption was measured using glucose oxidase method, and the expression and the acute translocation of GLUT4 was detected by Western-blot. The activity of AKT kinase was analyzed by immunoprecipitation （IP） coupled with Western blot. Results Mangiferin could up regulate the AKT kinase activity compared with control group （P〈0.01）, and enhance the glucose consumption in L6 cells （P=0. 011 or P =0. 000） in a dose response relationship （P=0. 000）. It also increased the protein expression of GLUT4 （P=0. 001 or P=O. 000） and promoted acute intracellular translocation of GLUT4 （P=0. 005; P=0. 001 or P=0. 026）, indicating that this protein translocated from the cytoplasm to the plasma membrane through the cytoskeleton system. Conclusions Mangiferin is able to enhance glucose consumption in L6 cell, increase the expression of GLUT4 and change the intracellular distribution of GLUT4, up-regulate the AKT kinase activity. Therefore it may have a potential auxiliary hypoglycemic effect.