Objective       To determine the effect of dihydromyricetin (DHM) on lipid metabolism in hepatic cells and its relationship with silent information regulator 1 (SIRT1) signaling pathway.       Methods       HepG2 cells were treated by 0.2 mmol/L palmitic acid (PA) for 24 h to establish a model of hepatic steatosis

and then followed by the treatment of 0

5

10 and 20 μmol/L DHM or 20 μmol/L DHM plus 2 μmol/L EX527 (SIRT1 inhibitor) for 24 h.CCK-8 assay was used to detect the cell viability

oil Red O staining was employed to detect the intracellular lipid droplets

enzyme-coupled colorimetric assay was adopted to measure triglyceride (TG) content

and Western blotting was used to detect the protein expression of SIRT1

adenosine monophosphate activated protein kinase (AMPK)

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

fatty acid synthetase (FAS) and acetyl-CoA carboxylase (ACC).       Results       The results indicated that 0.2 mmol/L PA as well as 5

10 and 20 μmol/L DHM had no significant effect on the proliferation of HepG2 cells (P0.05)

while 5

10 and 20 μmol/L DHM significantly reduced the accumulation of lipid droplets and level of TG in HepG2 cells

increased the protein expression levels of P-AMPK and SIRT1

and at the same time

reduced the protein levels of SREBP-1c

FAS and p-ACC. SIRT1 inhibitor

EX527

significantly increased the TG level (P0.01)

and weakened the reducing effect of DHM on the levels of SREBP-1c

FAS and p-ACC in HepG2 cells.       Conclusion       DHM improves hepatocyte fatty degeneration by up-regulating SIRT1 signaling pathway.