The effect of inflammatory cytokines in alcoholic liver disease.

The effect of inflammatory cytokines in alcoholic liver disease.
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DOI:
10.1155/2013/495156
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发表时间:
2013
影响因子:
4.6
通讯作者:
Fukui H
Fukui H
中科院分区:
医学3区
文献类型:
--
作者:
Kawaratani H;Tsujimoto T;Douhara A;Takaya H;Moriya K;Namisaki T;Noguchi R;Yoshiji H;Fujimoto M;Fukui H

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酒精是世界上最常见的肝病病因。长期饮酒会导致肝细胞损伤和肝脏炎症。炎性细胞因子如肿瘤坏死因子-α和干扰素-γ可诱导酒精性肝病大鼠的肝损伤。保护肝脏的细胞因子,如IL-6和抗炎细胞因子,如IL-10,也与ALD有关。IL-6通过激活信号转导和转录激活因子3(STAT3)以及随后在肝细胞中诱导多种肝保护基因来改善ALD。IL-10通过激活枯否细胞中的STAT3抑制酒精性肝脏炎症。饮酒通过增加肠源性内毒素转位到门静脉循环,并通过脂多糖/Toll样受体(TLR)4途径激活Kupffer细胞来促进肝脏炎症。氧化应激和微生物区系产物也与ALD有关。促炎和抗炎细胞因子与其他细胞因子和趋化因子之间的相互作用可能在ALD的发生发展中发挥重要作用。本研究旨在从炎症的角度对ALD进行系统综述。
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.
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