Institute for Liver and Digestive Disease, College of Medicine, Hallym University, Chuncheon 24253, Korea.
Int J Mol Sci. 2022 Aug 6;23(15):8749. doi: 10.3390/ijms23158749.
Alcohol consumption is a global healthcare problem. Chronic alcohol consumption generates a wide spectrum of hepatic lesions, the most characteristic of which are steatosis, hepatitis, fibrosis, and cirrhosis. Alcoholic liver diseases (ALD) refer to liver damage and metabolomic changes caused by excessive alcohol intake. ALD present several clinical stages of severity found in liver metabolisms. With increased alcohol consumption, the gut microbiome promotes a leaky gut, metabolic dysfunction, oxidative stress, liver inflammation, and hepatocellular injury. Much attention has focused on ALD, such as alcoholic fatty liver (AFL), alcoholic steatohepatitis (ASH), alcoholic cirrhosis (AC), hepatocellular carcinoma (HCC), a partnership that reflects the metabolomic significance. Here, we report on the global function of inflammation, inhibition, oxidative stress, and reactive oxygen species (ROS) mechanisms in the liver biology framework. In this tutorial review, we hypothetically revisit therapeutic gut microbiota-derived alcoholic oxidative stress, liver inflammation, inflammatory cytokines, and metabolic regulation. We summarize the perspective of microbial therapy of genes, gut microbes, and metabolic role in ALD. The end stage is liver transplantation or death. This review may inspire a summary of the gut microbial genes, critical inflammatory molecules, oxidative stress, and metabolic routes, which will offer future promising therapeutic compounds in ALD.
饮酒是一个全球性的医疗保健问题。慢性饮酒会导致广泛的肝损伤,其中最典型的是脂肪肝、肝炎、纤维化和肝硬化。酒精性肝病(ALD)是指由于过量饮酒导致的肝脏损伤和代谢组学变化。ALD 在肝脏代谢中表现出几个严重程度的临床阶段。随着饮酒量的增加,肠道微生物群会导致肠道渗漏、代谢功能障碍、氧化应激、肝脏炎症和肝细胞损伤。人们对 ALD 给予了高度关注,例如酒精性脂肪肝(AFL)、酒精性脂肪性肝炎(ASH)、酒精性肝硬化(AC)、肝细胞癌(HCC),这种关联反映了代谢组学的重要意义。在这里,我们报告了炎症、抑制、氧化应激和活性氧(ROS)机制在肝脏生物学框架中的全球功能。在本教程综述中,我们假设性地回顾了治疗性肠道微生物群衍生的酒精性氧化应激、肝脏炎症、炎症细胞因子和代谢调节。我们总结了微生物治疗基因、肠道微生物和 ALD 代谢作用的观点。终末期是肝移植或死亡。本综述可能会激发对肠道微生物基因、关键炎症分子、氧化应激和代谢途径的总结,这将为 ALD 提供有前途的治疗化合物。