Retracted: Kweichow Moutai ameliorates alcohol‐induced liver fibrosis in mice by targeting the NFκB pathway

Abstract

Previous epidemiological and histopathological studies have demonstrated that long‐term computation of Kweichow Moutai liquor (Moutai) could induce fatty liver disease but few of these patients with fatty liver will develop hepatic fibrosis or cirrhosis. Moutai liquor has a different brewing technique from other white wine, which may generate various microorganisms in the unique geographical conditions and may produce plenty of vitamins, amino acids, and several essential microelements. In the current study, we evaluated the potential protective effect of Moutai liquor in alcohol‐induced liver fibrosis mouse model. Both in vivo and in vitro studies were performed for exploring the possible mechanisms in suppressing liver fibrosis by Moutai. We demonstrated that Moutai treatment induced hepatic stellate cell (HSC) apoptosis and suppressed collagen deposition, as well as attenuated hepatic fibrosis. The antifibrosis mechanism of Moutai was possibly related with the inhibition of Kupffer cell and HSC activation via suppressing NFκB nuclear translocation and preventing the expression of pro‐inflammatory cytokines. It is worth noting that although Moutai attenuates liver fibrosis, it still causes lipid metabolic abnormalities in mouse liver and induces fatty liver. Kweichow Moutai may ameliorate alcohol‐induced liver fibrosis in mice by targeting the NFκB pathway.

Small-molecule natural products for reversing liver fibrosis based on modulation of HSCs activation: an update

“…2.8 Toll-like receptor 4 (TLR4) signaling pathway TLR4 is recognized by exogenous ligands, bacterial lipopolysaccharides and lipoproteins, as well as endogenous damage-related pattern ligands such as high mobility group protein B1 (HMGB1), as well as is involved in host immune regulation and inflammatory responses, and sensitizes the TGF-β pathway in HSCs though downregulating the expression of TGF-β pseudo receptor bone morphogenetic proteins and activin transmembrane inhibitors. NF-κB is a transcription factor downstream of TLR4 signaling that migrates to the nucleus upon activation and upregulates TGF-β1 expression [129] . TLR-2 is a direct binding receptor for hepatitis B e antigen (HBeAg).…”