Lee Eun-Ho, Seo Min-Hee, Park Soo-Young, Mukherjee Sulagna, Lee Jae-Ho, Kang Sora, Lee Ji-Yu, Lee Namgyu, Kwon Hung Taeck, Im Seung-Soon
Department of Physiology, Keimyung University School of Medicine, Daegu, Republic of Korea.
Department of Physiology, College of Medicine and Institute of Medical Sciences, Gyeongsang National University, Jinju, Korea.
PLoS One. 2025 Jul 10;20(7):e0327648. doi: 10.1371/journal.pone.0327648. eCollection 2025.
Alcohol-induced fatty liver disease is a significant contributor to global mortality, primarily resulting from excessive alcohol consumption and subsequent hepatic damage. This study investigated the therapeutic potential of MF001, an aldehyde-reducing compound derived from the yeast Saccharomyces cerevisiae in alcohol-induced liver damage. Using a Lieber-DeCarli ethanol diet-induced live disease model, we assessed the effects of MF001 on lipogenesis, oxidative stress, and inflammation. MF001 treatment significantly reduced lipid accumulation, as indicated by decreased expression of lipogenic genes. Moreover, MF001 suppresses reactive oxygen species (ROS) production indicated by reduced malondialdehyde levels and ROS-associated inflammatory markers, including Tnf-α, Il-6, and Mcp-1. Histological analysis revealed decreased hepatic lipid deposition and inflammation following MF001 administration. Furthermore, MF001 modulated alcohol metabolism by downregulating Cyp2e1 and Adh1, thereby decreasing acetaldehyde accumulation and improving liver function, as evidenced by normalized ALT and AST levels. Our findings suggest that MF001 alleviates alcohol-induced liver damage through its anti-inflammatory, antioxidant, and lipid-lowering properties, highlighting its potential as a function agent for preventing and treating alcohol-induced fatty liver disease.
酒精性脂肪肝病是全球死亡率的一个重要因素，主要由过量饮酒及随后的肝损伤所致。本研究调查了MF001（一种源自酿酒酵母的醛还原化合物）在酒精性肝损伤中的治疗潜力。利用Lieber-DeCarli乙醇饮食诱导的肝病模型，我们评估了MF001对脂肪生成、氧化应激和炎症的影响。MF001治疗显著减少了脂质积累，这由脂肪生成基因表达的降低所表明。此外，MF001抑制了活性氧（ROS）的产生，这由丙二醛水平降低以及包括Tnf-α、Il-6和Mcp-1在内的与ROS相关的炎症标志物所表明。组织学分析显示，给予MF001后肝脏脂质沉积和炎症减少。此外，MF001通过下调Cyp2e1和Adh1来调节酒精代谢，从而减少乙醛积累并改善肝功能，这由正常化的ALT和AST水平所证明。我们的研究结果表明，MF001通过其抗炎、抗氧化和降脂特性减轻酒精性肝损伤，突出了其作为预防和治疗酒精性脂肪肝病的功能剂的潜力。
