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目的研究槲皮素对棕榈酸(PA)诱导的胰岛素抵抗HepG2细胞糖代谢的改善作用。方法用棕榈酸诱导的HepG2细胞建立胰岛素抵抗模型。用MTT法观察不同浓度槲皮素对HepG2细胞的影响,用葡萄糖氧化酶法检测葡萄糖消耗,用实时PCR(Real-time PCR)的方法检测AKT、GSK-3β、G6Pase、GCK的基因表达,用免疫印迹法(Western blotting)检测AKT、GSK-3β的磷酸化蛋白表达及G6Pase、GCK的蛋白表达。结果槲皮素能够增加棕榈酸诱导HepG2细胞中的葡萄糖消耗,明显增加棕榈酸诱导HepG2细胞中AKT的磷酸化水平,降低GSK-3β磷酸化水平,降低G6Pase基因和蛋白表达,增加GCK基因和蛋白表达。结论槲皮素能改善棕榈酸诱导的胰岛素抵抗HepG2细胞的糖代谢作用,与其激活AKT信号通路密切相关。
Objective To study the effect of quercetin on the improvement of glycometabolism in insulin-resistant HepG2 cells induced by palmitic acid (PA). Methods Palmitic acid-induced HepG2 cells were used to establish insulin resistance model. The effects of different concentrations of quercetin on HepG2 cells were observed by MTT assay. The glucose consumption was measured by glucose oxidase method. The gene expressions of AKT, GSK-3β, G6Pase and GCK were detected by real-time PCR. The phosphorylation of AKT and GSK-3β and the expression of G6Pase and GCK were detected by Western blotting. Results Quercetin could increase the glucose consumption induced by palmitate in HepG2 cells and significantly increase the phosphorylation of AKT in HepG2 cells induced by palmitate, decrease the phosphorylation of GSK-3β, decrease the expression of G6Pase gene and protein, increase the expression of GCK gene and protein expression. Conclusion Quercetin can improve palmitate-induced glucose metabolism in HepG2 cells, which is closely related to its activation of AKT signaling pathway.