生脉散对HepG2细胞胰岛素抵抗的改善作用及其机制

Improving effect and its mechanism of Shengmai San on insulin-resistant HepG2 cells

目的探讨生脉散对HepG2细胞胰岛素抵抗的改善作用及其机制。方法建立HepG2细胞胰岛素抵抗模型,分别用葡萄糖氧化酶法、RT-PCR、Western blot检测生脉散对HepG2细胞葡萄糖代谢、PPARγ表达的影响。结果与模型组和吡格列酮组比较,生脉散组HepG2细胞上清液中葡萄糖含量降低,细胞内糖原含量增高(P<0.01或0.05)。吡格列酮组和生脉散组PPARγ表达高于模型组(P<0.01),但高剂量生脉散组与吡格列酮组差异无统计学意义(P>0.05)。结论生脉散可改善胰岛素抵抗HepG2细胞的糖代谢,其机制可能与上调PPARγ表达有关。

Objective To investigate the improving effect and its mechanism of Shengmai San（SMS） on insulin-resistant HepG2 cells.MethodsThe insulin resistance model of HepG2 cells was established.The effect of SMS on glucose metabolism and PPARγ expression in HepG2 cells was detected by glucose oxidase assay,RT-PCR and Western blot,respectively.Results Compared with model and pioglitazone groups,glucose content in the supernatant of HepG2 cells was decreased,while intracellular glycogen level increased in SMS group（P〈0.01 or 0.05）.PPARγ expression was higher in SMS and pioglitazone groups than in model group（P〈0.01）,but it was insignificant between high-dose SMS and pioglitazone groups（P〉0.05）.Conclusion SMS may improve insulin resistance of HepG2 cells through upregulating PPARγ expression.