Objective      To investigate the possible mechanism of mangiferin in ameliorating high-fructose-induced triglyceride (TG) deposition in HepG2 cells.       Methods      HepG2 cells were cultured in Dulbecco minimum essential medium with low fructose concentration (1 g/L glucose)

and then the cells were divided into control group (no fructose)

fructose group (30 mmol/L fructose)

and fructose+mangiferin groups with different concentrations (6.25

12.5

25 and 50 μmol/L) of mangiferin. After intervention for 24 h

the lipid droplet deposition was observed by oil red O staining

and the content of triglyceride was detected by enzymatic method. Real-time PCR was used to determine the mRNA expression of carbohydrate response element binding protein (ChREBP)

sterol regulatory element binding protein-1c (SREBP-1c)

liver pyruvate kinase (LPK) and diacylglycerol acyltransferase-2 (DGAT-2).       Results      Compared with the control group

HepG2 cells in the fructose group showed more lipid droplets and higher TG content (P0.05). Compared with the fructose group

low doses of mangiferin had no effect on the lipid droplet deposition caused by fructose

while high doses of mangiferin (25 and 50 μmol/L) decreased lipid droplets and TG content significantly (P0.05)

of which 50 μmol/L mangiferin exhibited the best intervention effect. Real-time PCR result showed that

compared with the control group

the mRNA expressions of ChREBP

SREBP-1c

LPK

and DGAT-2 increased significantly in the fructose group. Although 50 μmol/L mangiferin could down-regulate the mRNA expressions of ChREBP

LPK

and DGAT-2 (P0.05)

it showed minimal effect on SREBP-1c mRNA expression.       Conclusion      Mangiferin ameliorates high-fructose-induced TG deposition in HepG2 cells through inhibiting over-expressions of lipid synthesis related genes including ChREBP

LPK and DGAT-2.