Myricitrin ameliorates ethanol-induced steatosis in mouse AML12 liver cells by activating AMPK, and reducing oxidative stress and expression of inflammatory cytokines.

It is necessary to identify compounds that may provide protection against alcoholic liver disease. To the best of our knowledge, the effect of myricitrin on the development of ethanol‑induced liver disease has not been previously investigated. The present study aimed to determine the effect of myricitrin on ethanol‑induced steatosis in AML12 mouse liver cells and to identify the underlying molecular mechanisms. Ethanol‑treated AML12 cells exhibited significant improvement in viability following treatment with myricitrin. Oil red O staining indicated that myricitrin ameliorated ethanol‑induced lipid accumulation in cells. Furthermore, following treatment with myricitrin, improvement in ethanol‑induced steatosis and decrease in the levels of reactive oxygen species and lipoperoxides were observed in ethanol‑stimulated cells. Myricitrin suppressed mRNA and protein expression of tumor necrosis factor‑α, interleukin‑6 and transforming growth factor‑β1 in ethanol‑stimulated AML12 cells. Myricitrin markedly increased phosphorylation of adenosine monophosphate‑activated protein kinase (AMPK) and significantly reduced mRNA expression of sterol‑regulatory element‑binding protein‑1c (SREBP‑1c) and fatty acid synthase in ethanol‑stimulated AML12 cells. The results of the present study indicate that myricitrin ameliorates ethanol‑induced steatosis in AML12 cells by attenuating oxidative stress, suppressing expression of certain inflammatory cytokines and modulating the AMPK/SREBP-1c pathway.