Endotoxemia and gut barrier dysfunction in alcoholic liver disease.
Endotoxemia and gut barrier dysfunction in alcoholic liver disease.
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DOI：
10.1002/hep.23009
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发表时间：
2009-08
期刊：
影响因子：
--
通讯作者：
Rao R
中科院分区：
文献类型：
--
作者：
Rao R
越来越多的证据表明内毒素血症与酒精性肝病（ALD）密切相关。内毒素通过toll样受体-4 （TLR-4）介导的机制刺激肝脏中不同的细胞释放细胞因子、趋化因子和活性氧（ROS）。肠道菌群是循环内毒素的来源，肠道屏障功能障碍导致肠道通透性升高被认为是ALD患者内毒素血症的主要原因。乙醇诱导肠道屏障破坏的机制是一个活跃的研究领域。有证据表明，肠道菌群、乙醇代谢和乙醛诱导的细胞信号传导参与了乙醇诱导的肠道屏障功能障碍。本文就酒精性内毒素血症的最新进展、上皮屏障破坏的机制以及预防酒精性内毒素血症的因素进行了讨论。目前对这些问题的理解见图1。
Agrowing body of evidence indicates that endotox-emia is closely associated with alcoholic liver disease (ALD). Endotoxins stimulate different cells in the liver releasing cytokines, chemokines, and reactive oxygen species (ROS) by toll-like receptor-4 (TLR-4)–mediated mechanisms. Intestinal microflora is the source of circulating endotoxins, and the gut barrier dysfunction leading to elevated intestinal permeability is considered the main cause of endotoxemia in ALD. The mechanism of ethanol-induced gut barrier disruption is an active area of investigation. Evidence indicates that intestinal microflora, the metabolism of ethanol, and acetaldehyde-induced cell signaling are involved in ethanol-induced intestinal barrier dysfunction. Recent advances in alcoholic endotoxemia, the mechanism of epithelial barrier disruption, and the factors that prevent alcoholic endotoxemia are discussed in this article. The current understanding of these issues is illustrated in Fig. 1.
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DOI：
10.1016/j.alcohol.2008.12.009
发表时间：
2009-03
期刊：
Alcohol (Fayetteville, N.Y.)
影响因子：
--
作者：
Forsyth CB;Farhadi A;Jakate SM;Tang Y;Shaikh M;Keshavarzian A
通讯作者：
Keshavarzian A
DOI：
10.1111/j.1440-1746.1995.tb01793.x
发表时间：
1995-01-01
影响因子：
4.1
作者：
FUKUI, H;KITANO, H;TSUJII, T
通讯作者：
TSUJII, T
影响因子：
4.1
作者：
Basuroy, S;Seth, A;Rao, R
通讯作者：
Rao, R
DOI：
10.1111/j.1530-0277.2000.tb00012.x
发表时间：
2000-04-01
影响因子：
3.2
作者：
Fujimoto, M;Uemura, M;Fukui, H
通讯作者：
Fukui, H
影响因子：
4.7
作者：
Homann, N;Tillonen, J;Salaspuro, M
通讯作者：
Salaspuro, M