糖肾方对HepG2细胞胰岛素抵抗的影响及其机制探讨

Discussion of the Effects and Mechanism of Tangshen Formula on Insulin-induced Insulin Resistant HepG2 Cells

目的:研究中药复方糖肾方对胰岛素抵抗HepG2细胞的影响,并初步探讨其对糖脂代谢重要信号通路PI3K/AKT/SREBP-1c的调节作用。方法:采用20μg·mL-1胰岛素体外诱导法建立胰岛素抵抗HepG2细胞模型,通过测定给药后细胞增殖、葡萄糖消耗、脂质蓄积、超氧化物歧化酶和丙二醛含量评价糖肾方对胰岛素抵抗HepG2细胞状态的影响。同时,采用实时荧光定量PCR定量测定PI3K/AKT/SREBP-1c通路中PI3K、AKT1、GLUT4、PPARα、SREBP-1c和FASN 6个关键因子的基因表达。结果:相较于模型组,糖肾方干预后,胰岛素抵抗HepG2细胞的葡萄糖消耗增加,细胞中超氧化物歧化酶含量增加,丙二醛含量和甘油三酯的蓄积减少;PI3K/AKT/SREBP-1c通路中PI3K、AKT1、GLUT4和PPARαmRNA表达显著上调,SREBP-1c和FASN表达显著下调。结论:糖肾方可以通过调控细胞的糖脂代谢异常,从而改善HepG2细胞的胰岛素抵抗状态,并且PI3K/AKT/SREBP-1c通路在此过程中发挥重要作用。

Objective To study the effects of Chinese herbal compound Tangshen formula on insulin resistance HepG2 cells, and to explore its regulation of PI3 K/AKT/SREBP-1 c, an important signaling pathway for glycolipid metabolism. Methods insulin-resistant HepG2 cells model was established by in vitor induction of 20 μg·mL-1 insulin. To evaluate the effect of Tangshen formula on insulin-resistance HepG2 cells status by measuring cell proliferation, glucose consumption, lipid accumulation, superoxide dismutase and malondialdehyde content after administration. At the same time, real-time quantitative PCR was used to quantify the gene expression of PI3 K, AKT1, GLUT4, PPARα, SREBP-1 c and FASN in the PI3 K/AKT/SREBP-1 c pathway. Results Compared with the model group,the glucose consumption of insulin-resistant HepG2 cells increased, the superoxide dismutase content in the cells increased, and the accumulation of malondialdehyde content and triglyceride decreased. And the expression of PI3 K, AKT1, GLUT4 and PPARα mRNA in PI3 K/AKT/SREBP-1 c pathway was significantly up-regulated, and the expression of SREBP-1 c and FASN m RNA was significantly down-regulated. Conclusion Tangshen formula can improve the insulin resistance of HepG2 cells by regulating abnormal glucose and lipid metabolism in cells, and the PI3 K/AKT/SREBP-1 c pathway plays an important role in this process.