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目的观察槲皮素-3-o-新橙皮糖苷对L6肌管细胞胰岛素抵抗模型葡萄糖消耗;脂肪酸消耗以及对PPARα、PPARγ、GLUT4表达量的调节作用及其作用机制。方法以250μmol/L的脂肪酸诱导形成L6肌管细胞胰岛素抵抗模型,以槲皮素-3-o-新橙皮糖苷干预24 h后,葡萄糖氧化酶法检测葡萄糖消耗量,气相色谱法(GC)检测脂肪酸消耗量,Western-blot方法检测细胞中葡萄糖转运蛋白4(GLUT4)以及PPARα、PPARγ的表达量。结果槲皮素-3-o-新橙皮糖苷处理可提高L6细胞对葡萄糖的消耗(P<0.01),降低细胞脂肪酸摄入(P<0.05),上调GLUT4和PPARγ蛋白表达量(分别为P<0.01和P<0.05),但对PPARα的表达量无明显影响。结论槲皮素-3-o-新橙皮糖苷可提高L6细胞胰岛素抵抗模型葡萄糖消耗量,降低脂肪酸摄入,调节PPARγ、GLUT4的表达,这些可能是受试物缓解胰岛素抵抗的机制之一。
Objective To investigate the effects of quercetin-3-o-neohesperidoside on glucose consumption, fatty acid consumption, and the regulation of PPARα, PPARγ and GLUT4 expression in L6 myotube insulin resistance model and its mechanism. Methods The insulin resistance model of L6 myotubes was induced by 250 μmol / L fatty acid. Glucose consumption was measured by glucose oxidase method after 24 h intervention with quercetin-3-o-neoglucoside. Gas chromatography (GC) The consumption of fatty acids was detected. The expression of glucose transporter 4 (GLUT4) and PPARα and PPARγ in cells were detected by Western-blot. Results The treatment with quercetin -3-o-neohesperidin increased the glucose consumption (P <0.01), decreased the cellular fatty acid intake (P <0.05) and up-regulated the expression of GLUT4 and PPARγ protein (P <0.01 and P <0.05), but no significant effect on the expression of PPARα. Conclusions Quercetin-3-o-neohesperidin can increase glucose consumption, decrease fatty acid intake and regulate the expression of PPARγ and GLUT4 in L6 insulin resistance model, which may be one of the mechanisms by which the test substance can relieve insulin resistance.