LAUSR

BACKGROUND This study aims to explore blueberry polyphenols and its roles in nonalcoholic fatty liver disease (NAFLD) by relieving hepatic steatosis, and to understand alcoholic fatty liver disease (AFLD). Cell autophagy has been proved to promote lipid metabolism and is involved in the pathogenesis of AFLD; however, whether blueberry polyphenol affects autophagy is unknown. Therefore, our study analyzes the functions of blueberry polyphenol on AFLD and if its mechanisms are engaged with hepatocytes autophagy. METHODS We built the AFLD mice model via alcohol abduction, and the TG lipid droplets content detected the hepatic steatosis through ORO and HE stains. For blood lipid levels measurements, serum CHOL and TG concentrations were tests. For mechanism analysis, the lipogenic genes of SREBP1, FAS, and ACCα, and the lipodieretic genes of ATGL and Sirt1 were evaluated by qRT-PCR, as well as the autophagy proteins of p62; WB measured LC3-I and LC3-II. RESULTS We found that chronic alcohol intake successfully induced AFLD occurrence with increased TG lipid droplets content in liver and serum CHOL and TG levels that accompanied by increased lipogenic and reduced lipodieretic mRNA levels, as well as enhancive p62 protein and decreased LC3-II/LC3-I proportion. However, after blueberry polyphenol intake, there were opposite outcomes happened. Moreover, blueberry polyphenol alone did not affect the lipid metabolism but promoted the hepatocytes autophagy at 200 mg/kg concentration. CONCLUSIONS In summary, we are unparalleled that illustrated blueberry polyphenols can prevent AFLD development by promoting autophagy to accelerate lipid metabolism than to lighten hepatic steatosis.