Third Department of Internal Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan.
Mediators Inflamm. 2013;2013:495156. doi: 10.1155/2013/495156. Epub 2013 Dec 9.
Alcohol is the most common cause of liver disease in the world. Chronic alcohol consumption leads to hepatocellular injury and liver inflammation. Inflammatory cytokines, such as TNF-α and IFN-γ, induce liver injury in the rat model of alcoholic liver disease (ALD). Hepatoprotective cytokines, such as IL-6, and anti-inflammatory cytokines, such as IL-10, are also associated with ALD. IL-6 improves ALD via activation of the signal transducer and activator of transcription 3 (STAT3) and the subsequent induction of a variety of hepatoprotective genes in hepatocytes. IL-10 inhibits alcoholic liver inflammation via activation of STAT3 in Kupffer cells and the subsequent inhibition of liver inflammation. Alcohol consumption promotes liver inflammation by increasing translocation of gut-derived endotoxins to the portal circulation and activating Kupffer cells through the LPS/Toll-like receptor (TLR) 4 pathways. Oxidative stress and microflora products are also associated with ALD. Interactions between pro- and anti-inflammatory cytokines and other cytokines and chemokines are likely to play important roles in the development of ALD. The present study aims to conduct a systemic review of ALD from the aspect of inflammation.
酒精是世界范围内导致肝脏疾病的最常见原因。慢性酒精摄入可导致肝细胞损伤和肝脏炎症。在酒精性肝病（ALD）大鼠模型中，炎性细胞因子如 TNF-α和 IFN-γ可诱导肝损伤。肝保护细胞因子如 IL-6 和抗炎细胞因子如 IL-10 也与 ALD 相关。IL-6 通过激活信号转导和转录激活因子 3（STAT3）并随后诱导肝细胞中多种肝保护基因的表达来改善 ALD。IL-10 通过在枯否细胞中激活 STAT3 并随后抑制肝脏炎症来抑制酒精性肝炎症。酒精摄入通过增加肠道来源的内毒素向门静脉循环的易位并通过 LPS/Toll 样受体（TLR）4 途径激活枯否细胞来促进肝脏炎症。氧化应激和微生物群落产物也与 ALD 相关。促炎和抗炎细胞因子以及其他细胞因子和趋化因子之间的相互作用可能在 ALD 的发展中发挥重要作用。本研究旨在从炎症角度对 ALD 进行系统综述。
