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本文引用的文献

1
Altered intestinal microbiota-host mitochondria crosstalk in new onset Crohn's disease.新发克罗恩病中肠道微生物群-宿主线粒体串扰的改变。
Nat Commun. 2016 Nov 23;7:13419. doi: 10.1038/ncomms13419.
2
Profound Chemopreventative Effects of a Hydrogen Sulfide-Releasing NSAID in the APCMin/+ Mouse Model of Intestinal Tumorigenesis.一种释放硫化氢的非甾体抗炎药在APCMin/+小鼠肠道肿瘤发生模型中的深度化学预防作用。
PLoS One. 2016 Feb 24;11(2):e0147289. doi: 10.1371/journal.pone.0147289. eCollection 2016.
3
A novel orally administered trimebutine compound (GIC-1001) is anti-nociceptive and features peripheral opioid agonistic activity and Hydrogen Sulphide-releasing capacity in mice.一种新型口服曲美布汀化合物(GIC-1001)具有抗伤害感受作用,在小鼠中具有外周阿片激动活性和硫化氢释放能力。
Eur J Pain. 2016 May;20(5):723-30. doi: 10.1002/ejp.798. Epub 2015 Nov 6.
4
Deciphering the pathogenesis of NSAID enteropathy using proton pump inhibitors and a hydrogen sulfide-releasing NSAID.使用质子泵抑制剂和一种释放硫化氢的非甾体抗炎药来阐明非甾体抗炎药肠病的发病机制。
Am J Physiol Gastrointest Liver Physiol. 2015 Jun 15;308(12):G994-1003. doi: 10.1152/ajpgi.00066.2015.
5
Hydrogen sulfide-based therapeutics: exploiting a unique but ubiquitous gasotransmitter.基于硫化氢的治疗方法:利用一种独特而普遍存在的气体递质。
Nat Rev Drug Discov. 2015 May;14(5):329-45. doi: 10.1038/nrd4433. Epub 2015 Apr 7.
6
Hydrogen sulfide protects from colitis and restores intestinal microbiota biofilm and mucus production.硫化氢可预防结肠炎,并恢复肠道微生物群生物膜和黏液生成。
Inflamm Bowel Dis. 2015 May;21(5):1006-17. doi: 10.1097/MIB.0000000000000345.
7
Hydrogen sulphide protects against NSAID-enteropathy through modulation of bile and the microbiota.硫化氢通过调节胆汁和微生物群来预防非甾体抗炎药相关性肠病。
Br J Pharmacol. 2015 Feb;172(4):992-1004. doi: 10.1111/bph.12961. Epub 2014 Nov 24.
8
Investigating the responses of Cronobacter sakazakii to garlic-drived organosulfur compounds: a systematic study of pathogenic-bacterium injury by use of high-throughput whole-transcriptome sequencing and confocal micro-raman spectroscopy.研究阪崎克罗诺杆菌对大蒜驱动的有机硫化合物的反应:利用高通量全转录组测序和共聚焦显微拉曼光谱系统研究病原菌损伤。
Appl Environ Microbiol. 2014 Feb;80(3):959-71. doi: 10.1128/AEM.03460-13. Epub 2013 Nov 22.
9
Enhanced synthesis and diminished degradation of hydrogen sulfide in experimental colitis: a site-specific, pro-resolution mechanism.实验性结肠炎中硫化氢的合成增强和降解减少:一种特定部位、促进分辨率的机制。
PLoS One. 2013 Aug 5;8(8):e71962. doi: 10.1371/journal.pone.0071962. Print 2013.
10
Diallyl trisulfide suppresses dextran sodium sulfate-induced mouse colitis: NF-κB and STAT3 as potential targets.二烯丙基三硫醚抑制葡聚糖硫酸钠诱导的小鼠结肠炎:NF-κB 和 STAT3 作为潜在靶点。
Biochem Biophys Res Commun. 2013 Jul 26;437(2):267-73. doi: 10.1016/j.bbrc.2013.06.064. Epub 2013 Jun 26.

硫化氢:微生物组-黏膜界面的稳定性调节剂。

Hydrogen sulfide: an agent of stability at the microbiome-mucosa interface.

机构信息

Department of Physiology and Pharmacology, University of Calgary , Calgary, Alberta , Canada.

Faculty of Medicine, Universidade Camilo Castelo Branco, Fernandópolis, Brazil.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2018 Feb 1;314(2):G143-G149. doi: 10.1152/ajpgi.00249.2017. Epub 2017 Oct 12.

DOI:10.1152/ajpgi.00249.2017
PMID:29025733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5866422/
Abstract

A diverse range of effects of the intestinal microbiota on mucosal defense and injury has become increasingly clear over the past decade. Hydrogen sulfide (HS) has emerged as an important mediator of many physiological functions, including gastrointestinal mucosal defense and repair. Hydrogen sulfide is produced by gastrointestinal tract tissues and by bacteria residing within the gut and can influence the function of a wide range of cells. The microbiota also appears to be an important target of hydrogen sulfide. HS donors can modify the gut microbiota, and the gastrointestinal epithelium is a major site of oxidation of microbial-derived HS. When administered together with nonsteroidal anti-inflammatory drugs, HS can prevent some of the dysbiosis those drugs induce, possibly contributing to the observed prevention of gastrointestinal damage. Exogenous HS can also markedly reduce the severity of experimental colitis and plays important roles in modulating epithelial cell-mucus-bacterial interactions in the intestine, contributing to its ability to promote resolution of inflammation and repair of tissue injury. In this paper we review recent studies examining the roles of HS in mucosal defense, the possibility that HS can damage the gastrointestinal epithelium, and effects of HS on the gut microbiota and on mucus and biofilm interactions in the context of intestinal inflammation.

摘要

在过去的十年中,肠道微生物群对黏膜防御和损伤的多种影响变得越来越清晰。硫化氢 (HS) 已成为许多生理功能的重要介质,包括胃肠道黏膜防御和修复。HS 由胃肠道组织以及肠道内的细菌产生,可以影响多种细胞的功能。微生物群似乎也是 HS 的一个重要靶点。HS 供体可以修饰肠道微生物群,而胃肠道上皮是微生物衍生 HS 氧化的主要部位。当与非甾体抗炎药一起给药时,HS 可以预防这些药物诱导的某些菌群失调,这可能有助于观察到的胃肠道损伤预防。外源性 HS 还可以显著减轻实验性结肠炎的严重程度,并在调节肠道上皮细胞-粘液-细菌相互作用方面发挥重要作用,有助于其促进炎症消退和组织损伤修复的能力。本文综述了最近研究 HS 在黏膜防御中的作用、HS 损伤胃肠道上皮的可能性,以及 HS 对肠道微生物群以及在肠道炎症背景下对粘液和生物膜相互作用的影响。