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Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin

Reactive oxygen species- (ROS-) mediated injury has been implicated in several inflammatory disorders, including inflammatory bowel disease (IBD). NADPH oxidases (NOXs) are the major source of endogenous ROS. Here, we investigated the role of NOXs derived-ROS in a mouse model of colitis induced by t...

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Autores principales: Mouzaoui, Souad, Djerdjouri, Bahia, Makhezer, Nesrine, Kroviarski, Yolande, El-Benna, Jamel, Dang, Pham My-Chan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167951/
https://www.ncbi.nlm.nih.gov/pubmed/25276054
http://dx.doi.org/10.1155/2014/312484
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author Mouzaoui, Souad
Djerdjouri, Bahia
Makhezer, Nesrine
Kroviarski, Yolande
El-Benna, Jamel
Dang, Pham My-Chan
author_facet Mouzaoui, Souad
Djerdjouri, Bahia
Makhezer, Nesrine
Kroviarski, Yolande
El-Benna, Jamel
Dang, Pham My-Chan
author_sort Mouzaoui, Souad
collection PubMed
description Reactive oxygen species- (ROS-) mediated injury has been implicated in several inflammatory disorders, including inflammatory bowel disease (IBD). NADPH oxidases (NOXs) are the major source of endogenous ROS. Here, we investigated the role of NOXs derived-ROS in a mouse model of colitis induced by the proinflammatory cytokine, tumor necrosis factor-α (TNF-α). Intraperitoneal injection of TNFα (10 μg · kg(−1)) induced an acute inflammation of the colon and a marked increase in expression of NADPH oxidase 1 (NOX1), a colon specific NADPH oxidase isoform. TNFα-induced colitis was also characterized by high production of keratinocyte-derived chemokine (KC) and mucosal infiltration of neutrophils, NOX2-expressing cells. Concomitantly, ROS production and lipid peroxidation were significantly enhanced while catalase activity and glutathione level were reduced indicating a redox imbalance in the colon. Furthermore, the redox-sensitive MAP kinases, ERK1/2 and p38 MAPK, were activated during TNFα-induced colitis. Pretreatment of mice with apocynin, an NADPH oxidase inhibitor with antioxidant properties, before TNFα challenge, prevented all these events. These data suggest that ROS derived from NADPH oxidases (mainly NOX1 and NOX2) and MAP kinase pathways could contribute to the induction and expansion of oxidative lesions characteristics of IBD and that apocynin could potentially be beneficial in IBD treatment.
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spelling pubmed-41679512014-09-28 Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin Mouzaoui, Souad Djerdjouri, Bahia Makhezer, Nesrine Kroviarski, Yolande El-Benna, Jamel Dang, Pham My-Chan Mediators Inflamm Research Article Reactive oxygen species- (ROS-) mediated injury has been implicated in several inflammatory disorders, including inflammatory bowel disease (IBD). NADPH oxidases (NOXs) are the major source of endogenous ROS. Here, we investigated the role of NOXs derived-ROS in a mouse model of colitis induced by the proinflammatory cytokine, tumor necrosis factor-α (TNF-α). Intraperitoneal injection of TNFα (10 μg · kg(−1)) induced an acute inflammation of the colon and a marked increase in expression of NADPH oxidase 1 (NOX1), a colon specific NADPH oxidase isoform. TNFα-induced colitis was also characterized by high production of keratinocyte-derived chemokine (KC) and mucosal infiltration of neutrophils, NOX2-expressing cells. Concomitantly, ROS production and lipid peroxidation were significantly enhanced while catalase activity and glutathione level were reduced indicating a redox imbalance in the colon. Furthermore, the redox-sensitive MAP kinases, ERK1/2 and p38 MAPK, were activated during TNFα-induced colitis. Pretreatment of mice with apocynin, an NADPH oxidase inhibitor with antioxidant properties, before TNFα challenge, prevented all these events. These data suggest that ROS derived from NADPH oxidases (mainly NOX1 and NOX2) and MAP kinase pathways could contribute to the induction and expansion of oxidative lesions characteristics of IBD and that apocynin could potentially be beneficial in IBD treatment. Hindawi Publishing Corporation 2014 2014-09-04 /pmc/articles/PMC4167951/ /pubmed/25276054 http://dx.doi.org/10.1155/2014/312484 Text en Copyright © 2014 Souad Mouzaoui et al. https://creativecommons.org/licenses/by/3.0/ 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
Mouzaoui, Souad
Djerdjouri, Bahia
Makhezer, Nesrine
Kroviarski, Yolande
El-Benna, Jamel
Dang, Pham My-Chan
Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title_full Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title_fullStr Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title_full_unstemmed Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title_short Tumor Necrosis Factor-α-Induced Colitis Increases NADPH Oxidase 1 Expression, Oxidative Stress, and Neutrophil Recruitment in the Colon: Preventive Effect of Apocynin
title_sort tumor necrosis factor-α-induced colitis increases nadph oxidase 1 expression, oxidative stress, and neutrophil recruitment in the colon: preventive effect of apocynin
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167951/
https://www.ncbi.nlm.nih.gov/pubmed/25276054
http://dx.doi.org/10.1155/2014/312484
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