Pleurotus citrinopileatus alleviates alcohol-induced fatty liver via upregulating AMPK signaling

OBJECTIVE The current study was designed to investigate the anti-steatosis effect of Pleurotus citrinopileatus extract(PC) and the underlying mechanism in vivo and in vitro.METHODS Acute and chronic alcoholic hepatosteatosis murine models and ethanol-treated HepG2 cells were applied.RESULTS In vitro,the anti-steatosis effect of PC was further confirmed via Nile red staining in HepG2 cells treated with ethanol.Both of acute and chronic alcohol-induced mice hepatosteatosis model,PC decreased serum aminotransferase and triglyceride accumulation.Upregulated sterol-regulatory element binding protein1(Srebp1),purinergic ligand-gated ion channel 7 receptor(P2 X7 R) and downregulated sirtuin1(SIRT1),adenosine 5′-monophosphate(AMP)-activated protein kinase α(AMPKα) caused by acute and chronic alcohol intake were modulated by PC.In ethanol-exposed HepG2 cells,PC reduced lipid accumulation in a concentration-dependent manner and exhibited superior ability in controlling lipid accumulation compared with metformin.CONCLUSION PC could abolish hepatic lipid accumulation through regulating SIRT1-AMPKα signaling in acute and chronic alcohol-induced hepatic steatosis.

OBJECTIVE The current study was designed to investigate the anti-steatosis effect of Pleurotus citrinopileatus extract （PC） and the underlying mechanism in vivo and in vitro. METHODS Acute and chronic alcoholic hepatosteatosis murine models and ethanol-treated HepG2 cells were applied. RESULTS In vitro, the anti-steatosis effect of PC was further confirmed via Nile red staining in HepG2 cells treated with ethanol. Both of acute and chronic alcohol-induced mice hepatosteatosis model, PC decreased serum aminotransferase and triglyceride accumulation. Upregulated sterol-regulatory element binding protein1 （Srebpl）, purinergic ligand-gated ion channel 7receptor （P2X7R） and downregulated sirtuinl （SIRT1）, adenosine 5＇-monophosphate （AMP）-activated protein kinase a （AMPKa） caused by acute and chronic alcohol intake were modulated by PC. In ethanol- exposed HepG2 cells, PC reduced lipid accumulation in a concentration-dependent manner and exhibited superior ability in controlling lipid accumulation compared with metformin. CONCLUSION PC could abolish hepatic lipid accumulation through regulating SIRT1-AMPKa signaling in acute and chronic alcohol-induced hepatic steatosis.