ABSTRACT
Objective To investigate the anti-hyperglycemic effect of the Chinese medicine ingredients such as berberine,baicalin,puerarin and liquiritin on the optimal insulin resistance (IR)-HepG2 cell model by oleic acid.It would provide the theoretical basis for the optimization of Chinese medicine prescription or anti-hyperglycemic components combination.Methods Different concentrations (0.1,0.2,0.5,and 1.0 mmol/L) of oleic acid were used to induce HepG2 cells for different time (24,36 and 48 h),the glucose consumption was measured byglucose oxidase assay,and cell viability was detected by CCK-8 assay to define the optimal inducing concentration and time for IR-HepG2 cell model.Then the cell morphological changes were detected by oil red O staining.Finally,the stability of IR-HepG2 cell model was tested.After the IR-HepG2 model was optimally established,the glucose consumption,glycogen content and cell viability were detected after 24 h administration with different concentrations of berberine,baicalin,puerarin and liquiritin by anthrone method,glycerol phosphate oxidase assay and CCK-8 assay respectively.Results The optimal oleic acid-induced concentration was 1 mmol/L and the optimal induced time was 24 h for the IR-HepG2 cell model that could keep stable more than 36 h.Comparing with IR model group,berberine,puerarin and baicalin significantly increased the glucose consumption,whereas liquiritin did not show significant change in the glucose consumption except for 1 μmol/L.Only 160 μmol/L puerarin and 1 μmol/L baicalin significantly inhibited IR-HepG2 cell viability.Moreover,berberine,puerarin,and baicalin significantly elevated the glycogen content;Liquiritin did not change glycogen content significantly.Conclusion The IR-HepG2 cell model could be stably established with 24 h treatment of 1 mmol/L oleic acid.Berberine,puerarin,and baicalin significantly increased the glucose consumption and glycogen content in the IR-HepG2 cells.The results suggest that berberine,baicalin and puerarin maybe perform different pathways of anti-hyperglycemic effects due to different incentives ofIR.