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肠-肝轴在肝硬化和门静脉高压发病机制中的作用。

The role of gut-liver axis in the pathogenesis of liver cirrhosis and portal hypertension.

机构信息

Gastroenterology Research Unit, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

Clin Mol Hepatol. 2012 Dec;18(4):337-46. doi: 10.3350/cmh.2012.18.4.337. Epub 2012 Dec 21.

DOI:10.3350/cmh.2012.18.4.337
PMID:23323248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3540369/
Abstract

Because of the anatomical position and its unique vascular system, the liver is susceptible to the exposure to the microbial products from the gut. Although large amount of microbes colonize in the gut, translocation of the microbes or microbial products into the liver and systemic circulation is prevented by gut epithelial barrier function and cleansing and detoxifying functions of the liver in healthy subjects. However, when the intestinal barrier function is disrupted, large amount of bacterial products can enter into the liver and systemic circulation and induce inflammation through their receptors. Nowadays, there have been various reports suggesting the role of gut flora and bacterial translocation in the pathogenesis of chronic liver disease and portal hypertension. This review summarizes the current knowledge about bacterial translocation and its contribution to the pathogenesis of chronic liver diseases and portal hypertension.

摘要

由于解剖位置及其独特的血管系统,肝脏容易受到肠道微生物产物的暴露。尽管大量的微生物定植在肠道中,但在健康受试者中,肠道上皮屏障功能和肝脏的清洁和解毒功能阻止了微生物或微生物产物向肝脏和全身循环的转移。然而,当肠道屏障功能被破坏时,大量的细菌产物可以进入肝脏和全身循环,并通过其受体引起炎症。现在,有各种报道表明肠道菌群和细菌易位在慢性肝病和门静脉高压症的发病机制中的作用。本综述总结了目前关于细菌易位及其对慢性肝病和门静脉高压症发病机制的贡献的知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/3540369/31c8836f60eb/cmh-18-337-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/3540369/31c8836f60eb/cmh-18-337-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/3540369/31c8836f60eb/cmh-18-337-g001.jpg

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Nature. 2012 Feb 1;482(7384):179-85. doi: 10.1038/nature10809.
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Lipopolysaccharide induces and activates the Nalp3 inflammasome in the liver.脂多糖诱导并激活肝脏中的 Nalp3 炎性体。
World J Gastroenterol. 2011 Nov 21;17(43):4772-8. doi: 10.3748/wjg.v17.i43.4772.
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