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Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so
Nitric oxide has been suggested as a contributor to tissue injury in various experimental models of gastrointestinal inflammation. However, there is overwhelming evidence that nitric oxide is one of the most important mediators of mucosal defence, influencing such factors as mucus secretion, mucosal...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
1995
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365665/ https://www.ncbi.nlm.nih.gov/pubmed/18475671 http://dx.doi.org/10.1155/S0962935195000640 |
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author | Kubes, Paul Wallace, John L. |
author_facet | Kubes, Paul Wallace, John L. |
author_sort | Kubes, Paul |
collection | PubMed |
description | Nitric oxide has been suggested as a contributor to tissue injury in various experimental models of gastrointestinal inflammation. However, there is overwhelming evidence that nitric oxide is one of the most important mediators of mucosal defence, influencing such factors as mucus secretion, mucosal blood flow, ulcer repair and the activity of a variety of mucosal immunocytes. Nitric oxide has the capacity to down-regulate inflammatory responses in the gastrointestinal tract, to scavenge various free radical species and to protect the mucosa from injury induced by topical irritants. Moreover, questions can be raised regarding the evidence purported to support a role for nitric oxide in producing tissue injury. In this review, we provide an overview of the evidence supporting a role for nitric oxide in protecting the gastrointestinal tract from injury. |
format | Text |
id | pubmed-2365665 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1995 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-23656652008-05-12 Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so Kubes, Paul Wallace, John L. Mediators Inflamm Research Article Nitric oxide has been suggested as a contributor to tissue injury in various experimental models of gastrointestinal inflammation. However, there is overwhelming evidence that nitric oxide is one of the most important mediators of mucosal defence, influencing such factors as mucus secretion, mucosal blood flow, ulcer repair and the activity of a variety of mucosal immunocytes. Nitric oxide has the capacity to down-regulate inflammatory responses in the gastrointestinal tract, to scavenge various free radical species and to protect the mucosa from injury induced by topical irritants. Moreover, questions can be raised regarding the evidence purported to support a role for nitric oxide in producing tissue injury. In this review, we provide an overview of the evidence supporting a role for nitric oxide in protecting the gastrointestinal tract from injury. Hindawi Publishing Corporation 1995-11 /pmc/articles/PMC2365665/ /pubmed/18475671 http://dx.doi.org/10.1155/S0962935195000640 Text en Copyright © 1995 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Kubes, Paul Wallace, John L. Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title | Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title_full | Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title_fullStr | Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title_full_unstemmed | Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title_short | Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so |
title_sort | nitric oxide as a mediator of gastrointestinal mucosal injury?—say it ain't so |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365665/ https://www.ncbi.nlm.nih.gov/pubmed/18475671 http://dx.doi.org/10.1155/S0962935195000640 |
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