大黄素激活AMPK、PPARγ对3T3-L1脂肪细胞葡萄糖摄取的影响

摘要

Aim To investigate glucose uptake effects and mechanism of emodin in 3T3-L1 adipocytes. Methods LPS-induced differentiated 3 T3-L1 adipo-cytes were divided into control group and emodin ( 1 , 10, 50 μmol · L-1 ) groups. Then, 6-NBDG uptake and the expression of cell surface GLUT4 , PPARγ, AMPKα1/2 , p-AMPKα1/2 , IRS-1 , p-IRS-1 , Adi-ponectin, chREBP-α and chREBP-β were detected. The ability of 6-NBDG uptake in LPS-induced 3 T3-L1 adipocytes was also evaluated following interference with AMPK inhibitor and PPARγinhibitor, respective-ly. Meanwhile, STZ-induced diabetic rats were ran-domly divided into control group and emodin treatment group. The mRNA expression of Adiponectin and pro-tein expression of cell surface GLUT4 , AMPKα1/2 , p-AMPKα1/2 were measured. Results Compared with the control group, emodin improved the mRNA expres-sion of cell surface GLUT4, Adiponectin, chREBP-αand chREBP-β, and protein expression of cell surface GLUT4 , PPARγ, IRS-1 , p-IRS-1 , AMPKα1/2 and p-AMPKα1/2 in 3T3-L1 adipocytes(P<0. 05). Emodin enhanced 6-NBDG uptake and the uptake of emodin group was both decreased following interference with AMPK inhibitor and PPARγ inhibitor, respectively ( P<0. 05 ) . Emodin also increased the mRNA expression of Adiponectin and protein expression of cell surface GLUT4 , AMPKα1/2 and p-AMPKα1/2 in adipose tis-sue of T2 DM rats ( P <0. 05 ) . Conclusion Emodin can enhance glucose uptake in 3 T3-L1 adipocytes and the mechanism is probably associated with activating Adiponectin and IRS-1 , thereby activating AMPK and PPARγ.%目的：研究大黄素对3 T3-L1脂肪细胞葡萄糖摄取的影响,并探讨其作用机制。方法诱导分化成熟的3 T3-L1脂肪细胞经LPS干预后分为Control组、大黄素给药组(1、10、50μmol · L-1),检测6-NBDG 摄取情况及 GLUT4、PPARγ、AMPKα1/2、p-AMPKα1/2、IRS-1、p-IRS-1、Adiponec-tin、chREBP-α和chREBP-β的表达。用AMPK和PPARγ抑制剂分别干预后,检测6-NBDG的摄取情况。同时,以 STZ诱导大鼠2型糖尿病模型,分为Control组和大黄素给药组,检测大鼠内脏脂肪组织的 Adiponectin 的 mRNA 表达及GLUT4、AMPKα1/2、p-AMPKα1/2蛋白表达。结果与Con-trol组相比,大黄素可促进 GLUT4、Adiponectin、chREBP-α、chREBP-β的mRNA表达及GLUT4、PPARγ、IRS-1、p-IRS-1、AMPKα1/2和p-AMPKα1/2的蛋白表达( P<0．05),可提高3T3-L1脂肪细胞对6-NBDG的摄取,经AMPK及PPARγ抑制剂分别干预后,大黄素对6-NBDG的摄取降低(P<0．05)。同时,大黄素可促进T2DM大鼠内脏脂肪组织Adiponectin的mRNA表达及GLUT4、AMPKα1/2和p-AMPKα1/2的蛋白表达(P<0．05)。结论大黄素可促进3T3-L1脂肪细胞的葡萄糖摄取功能,其作用机制与激活 Adiponectin及 IRS-1,进而激活AMPK和PPARγ的信号通路有关。