洋甘菊总黄酮改善IR-HepG2细胞的作用机制

Mechanism of chamomile total flavonoids in improving IR-HepG2 cells

目的:探究洋甘菊总黄酮对HepG2胰岛素抵抗细胞氧化应激损伤的保护作用。方法:用17.5 mmol·L-1的葡萄糖胺诱导HepG2细胞24 h建立体外HepG2细胞胰岛素抵抗模型;通过CCK-8法测定不同浓度的洋甘菊总黄酮对HepG2细胞活力的影响;采用试剂盒测定葡萄糖(GLU)消耗量、细胞糖原含量和丙二醛(MDA)的含量,以及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性;Western blot法测定IRS1/PI3K/Akt通路关键信号分子蛋白的表达水平。结果:与模型组相比,洋甘菊总黄酮干预后细胞葡萄糖消耗量增加,细胞内糖原含量增多,MDA含量降低,SOD和GSH-Px酶活性升高,氧化应激损伤减轻;IRS1、PI3K和Akt等蛋白的磷酸化水平升高,葡萄糖转运蛋白4(GLUT4)表达上调(P<0.05)。结论:洋甘菊总黄酮可能通过调节IRS1/PI3K/Akt通路和GLUT4蛋白的表达来降低氧化应激损伤和抑制糖异生,从而改善细胞胰岛素抵抗。

OBJECTIVE To explore the pharmacological effect of chamomile flavonoids on oxidative stress injury of HepG2 insulin resistance cells.METHODS The insulin resistance model of HepG2 cells in vitro was established by 17.5 mmol·L-1 glucosamine inducing HepG2 cells for 24 h.The concentrations of chamomile total flavonoids on the viability of HepG2 cells were determinated by CCK-8 method.The contents of glucose consumption,cell glycogen content,SOD,MDA,GSH-Px were done with related kits.The protein expression of the key signaling molecules in the IRS-1/PI3K/Akt pathway in HepG2 cells were tested by Western blot.RESULTS Compared with the model group,the glucose consumption of cells and the intracellular glycogen contents were increased,MDA content was decreased,SOD and GSH-Px enzyme activity was increased,and the oxidative stress injurs were reduced.The level of IRS1,PI3K and Akt Phosphorylation of HepG2 Cells increased,and the expression of GLUT4 protein was up-regulated(P<0.05).CONCLUSION Chamomile total flavonoids regulate glycolytic metabolism,alleviate oxidative stress and insulin resistance by regulating the IRS1/PI3K/Akt signaling pathway and GLUT4 expression.