Effects of conditioned media for rat bone marrow-derived mesenchymal stem cells on palmitic acid-induced insulin resistance in HepG2 cells
10.3760/cma.j.issn.0578-1426.2015.05.013
- VernacularTitle:大鼠骨髓间充质干细胞条件培养基对HepG2细胞胰岛素抵抗的影响
- Author:
Xiaoya SUN
;
Haojie HAO
;
Weidong HAN
;
Yiming MU
- Publication Type:Journal Article
- Keywords:
Mesenchymal stem cells;
Insulin resistance;
HepG2 cells
- From:
Chinese Journal of Internal Medicine
2015;54(5):439-444
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of conditioned media for rat bone marrow mesenchymal stem cells (BMSCs-CM) on palmitic acid (PA)-induced insulin resistance (IR) in HepG2 cells and its underlying molecular mechanisms.Methods HepG2 cells were treated with or without BMSCs-CM and L-DMEM in the presence or absence of PA.Glucose utilization in HepG2 cells were detected with PAS,glucose and glycogen measurements.Western blotting was used to assess the expression of phospho-insulin receptor substrate (p-IRS),phosphatidylinositol 3-kinase (PI3 K) and p-AKT.Results (1) Incubation of HepG2 cells with 0.25 mmol/L PA for 24 hours significantly increased the glucose concentration and decreased the glycogen content (P ＜ 0.05) in the media.(2) Treatment with BMSCs-CM significantly ameliorated the glucose and glycogen alteration in cells pretreated with PA (P ＜ 0.05),however,no obvious effect of BMSCs-CM on the cell glucose and glycogen production.(3) BMSCs-CM treatment also increased protein expression of p-IRS,PI3K and p-AKT in PA incubated HapG2 cells (P＜ 0.05).The effect of BMSCs-CM on PI3K and p-AKT expression could be mimicked upon addition of 740Y-P,a PI3K agonist,but abolished by LY294002,a PI3K specific inhibitor.Conclusions BMSCs-CM could improve the insulin sensitivity in HepG2 cells pretreated with PA through upregulation of insulin signaling component expression.
