槲皮素-3-o-新橙皮糖苷改善 L6 细胞胰岛素抵抗及其作用机制

Effect of quercetin-3-o-neohesperidin on improving insulin resistance and its molecular mechanism

中文关键词:  槲皮素-3-o-新橙皮糖苷  葡萄糖转运蛋白 4  PPAR  胰岛素抵抗

英文关键词:quercetin-3-o-neohesperidin  GLUT4  PPAR  insulin resistance

中文摘要:

      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 250 μmol/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。

英文摘要:

      Objective To detect the effect of quercetin-3-o-neohesperidin on glucose consumption and fatty acid consumption and the expression of PPARα, PPAR, GLUT4 in L6 insulin resistance cell model, and then analyze its molecular mechanism. Methods The L6 myotube cells were derivated by 250 μmol/L free fatty acid to establish the insulin resistance cell model, then were intervened by quercetin-3-o-neohesperidin for 24 h. The glucose consumption and fatty acid consumption were measured by glucose oxidase method and GC respectively. The expression of GLUT4, PPARα, PPARγ were detected by Western-blot. Results Quercetin-3-o-neohesperidin increased the glucose consumption (P<0.01) and decreased the fatty acid consumption (P<0.05) in L6 cells, and up-regulated the protein expression of GLUT4, PPARγ (P<0.01, P<0.05 respectively). However, quercetin-3-o-neohesperidin did not show any significant impact on theexpression of PPARα between groups. Conclusion Quercetin-3-o-neohesperidin increase glucose consumption and decrease the fatty acid consumption in L6 insulin resistance cell model, up-regulate the protein expression of GLUT4 and PPARγ. Quercetin-3-o-neohesperidin plays a potential hypoglycemic and insulin sensitivity-improving effect.