Hepatic steatosis, characterized by excessive lipid accumulation in the liver, can be ameliorated by autophagy activation. Polygoni Cuspidati rhizome et Radix (PCRR), traditionally used to treat atherosclerosis, hepatitis, and gallstones, has recently demonstrated anti-steatotic effects in the liver. However, the active compounds and underlying mechanisms remain unclear. This study investigated whether PCRR water extract improves steatosis by modulating hepatic autophagic flux. We found that PCRR water extract promoted autophagic flux, enhanced lysosomal biogenesis, and alleviated lipid accumulation in the liver cell lines as well as in the livers of rats with steatosis. Mechanistically, PCRR water extract inhibited mechanistic target of rapamycin complex 1 (mTORC1) activity, leading to dephosphorylation and subsequent nuclear translocation of transcription factor EB (TFEB), a key regulator of lipophagy. TFEB knockdown attenuated PCRR-mediated lipophagy promotion in the liver cell lines. Furthermore, chloroquine (CQ)-mediated autophagy blockage abrogated the therapeutic effect of PCRR against hepatic steatosis in high-fat diet (HFD)-fed rats. These findings suggest that PCRR water extract acts as a novel autophagy enhancer and holds therapeutic potential for hepatic steatosis.

Alcoholic beverages are among the most widely enjoyed leisure drinks around the world. However, irresponsible drinking habits can have detrimental effects on human health. Therefore, exploring strategies to alleviate discomfort following alcohol consumption would be beneficial for individuals who inevitably need to consume alcohol. In this study, three different models were used to determine the efficacy of a patented alcohol degradation protein (ADP) extracted from Bos taurus on ethanol metabolism. In an ethanol-challenged HepG2 cell model, ADP significantly protected the cell from ethanol-induced toxicity. Subsequently, results demonstrated that ADP significantly alleviated the effect of ethanol, as reflected by the increased distance and activity time of zebrafish during the testing period. Additionally, in a rat model, ADP promoted ethanol degradation at 1 and 2 h after ethanol consumption. Mechanistic studies found that ADP treatment increased ADH and ALDH activity in the gastrointestinal tract. ADP also exhibited potent antioxidation effects by lowering HO-1 expression in the liver. In conclusion, we believe that ADP is a promising product for relieving hangover symptoms after ethanol consumption, with demonstrated safety and effectiveness at the recommended dosage.