Abstract: OBJECTIVE:To explore the impact of iron overload on iron metabolism index of Hepcidin and Fpn-1 in HepG2 cells,a model of nonalcoholic fatty liver disease (NAFLD). METHODS:Cell viability was determined using the MTT assay at different concentrations (0.062 5,0.125,0.25,0.5,1.0,2.0 mmol/L,respectively) of oleic acid (OA) and iron and to determine the combined drug concentration. The model of NAFLD was established by using 0.5 mmol/L OA in combination with different concentrations (0,0.125,0.25,0.5 mmol/L) of the Fe induced in HepG2 cells. The contents of intracellular triglyceride (TG) and ferritin (Fn) were determined. The mRNA levels of Hepcidin and Ferroportin1 (Fpn-1) were determined by quantitative real-time PCR and the protein expression of Hepcidin and Fpn-1 were determined by Western blot. A negative control group (no drug treatment of cells) and a 0.5 mmol/L Fe group were used as controls. RESULTS:Compared with the negative control group,0.5 mmol/L OA,0.125,0.25,0.5 mmol/L Fe had no obvious effect on cell viability (P > 0.05). Compared with the control and the 0.5 mmol/L OA groups,in groups of 0.5 mmol/L OA joint with various concentrations of Fe and with increased of the concentration of iron,intracellular TG and ferritin (Fn) content increased gradually and significantly (P < 0.05). Compared with the control and the 0.5 mmol/L OA group,the joint effect of 0.5 mmol/L OA with various concentrations of Fe resulted in the decrease of mRNA and protein expression of Hepcidin (P < 0.05),resulted in the increase of mRNA of Fpn-1 (P < 0.05). Compared with the control,0.5 mmol/L Fe group,0.5 mmol/L OA combined with 0.25 and 0.5 mmol/L Fe resulted in the decrease of protein expression of Fpn-1 (P < 0.05). CONCLUSION:The joint effect of 0.5 mmol/L OA with various concentrations of Fe aggravated the pathogenesis of NAFLD through lipid deposition and iron dysfunction.

Key words: iron overload, ferritin, iron metabolism, nonalcoholic fatty liver disease, Hepcidin, Fpn