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Melatonin Reduces Inflammatory Injury Through Inhibiting NF-κB Activation in Rats With Colitis
Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-κB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-κB in rats with colitis. Rat colitis model was establish...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2005
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1526481/ https://www.ncbi.nlm.nih.gov/pubmed/16192667 http://dx.doi.org/10.1155/MI.2005.185 |
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author | Li, Jun-Hua Yu, Jie-Ping Yu, Hong-Gang Xu, Xi-Ming Yu, Liang-Liang Liu, Jin Luo, He-Sheng |
author_facet | Li, Jun-Hua Yu, Jie-Ping Yu, Hong-Gang Xu, Xi-Ming Yu, Liang-Liang Liu, Jin Luo, He-Sheng |
author_sort | Li, Jun-Hua |
collection | PubMed |
description | Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-κB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-κB in rats with colitis. Rat colitis model was established by TNBS enema. NF-κB p65, TNF-α, ICAM-1, and IκBαin colon tissue were examined by immunohistochemistry, EMSA, RT-PCR, and Western blot analysis. Expression of proinflammatory molecule and activation of NF-κB were upregulated and IκB level decreased in rats with colitis. Melatonin reduces colonic inflammatory injury through downregulating proinflammatory molecule mediated by NF-κB inhibition and blockade of IκBα degradation. |
format | Text |
id | pubmed-1526481 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-15264812006-08-21 Melatonin Reduces Inflammatory Injury Through Inhibiting NF-κB Activation in Rats With Colitis Li, Jun-Hua Yu, Jie-Ping Yu, Hong-Gang Xu, Xi-Ming Yu, Liang-Liang Liu, Jin Luo, He-Sheng Mediators Inflamm Research Communication Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-κB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-κB in rats with colitis. Rat colitis model was established by TNBS enema. NF-κB p65, TNF-α, ICAM-1, and IκBαin colon tissue were examined by immunohistochemistry, EMSA, RT-PCR, and Western blot analysis. Expression of proinflammatory molecule and activation of NF-κB were upregulated and IκB level decreased in rats with colitis. Melatonin reduces colonic inflammatory injury through downregulating proinflammatory molecule mediated by NF-κB inhibition and blockade of IκBα degradation. Hindawi Publishing Corporation 2005-08-31 /pmc/articles/PMC1526481/ /pubmed/16192667 http://dx.doi.org/10.1155/MI.2005.185 Text en Hindawi Publishing Corporation |
spellingShingle | Research Communication Li, Jun-Hua Yu, Jie-Ping Yu, Hong-Gang Xu, Xi-Ming Yu, Liang-Liang Liu, Jin Luo, He-Sheng Melatonin Reduces Inflammatory Injury Through Inhibiting NF-κB Activation in Rats With Colitis |
title | Melatonin Reduces Inflammatory Injury Through Inhibiting
NF-κB Activation in Rats With Colitis |
title_full | Melatonin Reduces Inflammatory Injury Through Inhibiting
NF-κB Activation in Rats With Colitis |
title_fullStr | Melatonin Reduces Inflammatory Injury Through Inhibiting
NF-κB Activation in Rats With Colitis |
title_full_unstemmed | Melatonin Reduces Inflammatory Injury Through Inhibiting
NF-κB Activation in Rats With Colitis |
title_short | Melatonin Reduces Inflammatory Injury Through Inhibiting
NF-κB Activation in Rats With Colitis |
title_sort | melatonin reduces inflammatory injury through inhibiting
nf-κb activation in rats with colitis |
topic | Research Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1526481/ https://www.ncbi.nlm.nih.gov/pubmed/16192667 http://dx.doi.org/10.1155/MI.2005.185 |
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