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Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats

Lipoic acid (LA) and N-acetylcysteine (NAC) are antioxidant and anti-inflammatory agents that have not yet been tested on mild ulcerative colitis (UC). This study aims to evaluate the action of LA and/or NAC, on oxidative stress and inflammation markers in colonic and hepatic rat tissues with mild U...

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Autores principales: Moura, Fabiana Andréa, de Andrade, Kívia Queiroz, de Araújo, Orlando Roberto Pimentel, Nunes-Souza, Valéria, Santos, Juliana Célia de Farias, Rabelo, Luiza Antas, Goulart, Marília Oliveira Fonseca
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124475/
https://www.ncbi.nlm.nih.gov/pubmed/27957238
http://dx.doi.org/10.1155/2016/4047362
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author Moura, Fabiana Andréa
de Andrade, Kívia Queiroz
de Araújo, Orlando Roberto Pimentel
Nunes-Souza, Valéria
Santos, Juliana Célia de Farias
Rabelo, Luiza Antas
Goulart, Marília Oliveira Fonseca
author_facet Moura, Fabiana Andréa
de Andrade, Kívia Queiroz
de Araújo, Orlando Roberto Pimentel
Nunes-Souza, Valéria
Santos, Juliana Célia de Farias
Rabelo, Luiza Antas
Goulart, Marília Oliveira Fonseca
author_sort Moura, Fabiana Andréa
collection PubMed
description Lipoic acid (LA) and N-acetylcysteine (NAC) are antioxidant and anti-inflammatory agents that have not yet been tested on mild ulcerative colitis (UC). This study aims to evaluate the action of LA and/or NAC, on oxidative stress and inflammation markers in colonic and hepatic rat tissues with mild UC, induced by dextran sodium sulfate (DSS) (2% w/v). LA and/or NAC (100 mg·kg·day(−1), each) were given, once a day, in the diet, in a pretreatment phase (7 days) and during UC induction (5 days). Colitis induction was confirmed by histological and biochemical analyses (high performance liquid chromatography, spectrophotometry, and Multiplex®). A redox imbalance occurred before an immunological disruption in the colon. NAC led to a decrease in hydrogen peroxide (H(2)O(2)), malondialdehyde (MDA) levels, and myeloperoxidase activity. In the liver, DSS did not cause damage but treatments with both antioxidants were potentially harmful, with LA increasing MDA and LA + NAC increasing H(2)O(2), tumor necrosis factor alpha, interferon gamma, and transaminases. In summary, NAC exhibited the highest colonic antioxidant and anti-inflammatory activity, while LA + NAC caused hepatic damage.
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spelling pubmed-51244752016-12-12 Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats Moura, Fabiana Andréa de Andrade, Kívia Queiroz de Araújo, Orlando Roberto Pimentel Nunes-Souza, Valéria Santos, Juliana Célia de Farias Rabelo, Luiza Antas Goulart, Marília Oliveira Fonseca Oxid Med Cell Longev Research Article Lipoic acid (LA) and N-acetylcysteine (NAC) are antioxidant and anti-inflammatory agents that have not yet been tested on mild ulcerative colitis (UC). This study aims to evaluate the action of LA and/or NAC, on oxidative stress and inflammation markers in colonic and hepatic rat tissues with mild UC, induced by dextran sodium sulfate (DSS) (2% w/v). LA and/or NAC (100 mg·kg·day(−1), each) were given, once a day, in the diet, in a pretreatment phase (7 days) and during UC induction (5 days). Colitis induction was confirmed by histological and biochemical analyses (high performance liquid chromatography, spectrophotometry, and Multiplex®). A redox imbalance occurred before an immunological disruption in the colon. NAC led to a decrease in hydrogen peroxide (H(2)O(2)), malondialdehyde (MDA) levels, and myeloperoxidase activity. In the liver, DSS did not cause damage but treatments with both antioxidants were potentially harmful, with LA increasing MDA and LA + NAC increasing H(2)O(2), tumor necrosis factor alpha, interferon gamma, and transaminases. In summary, NAC exhibited the highest colonic antioxidant and anti-inflammatory activity, while LA + NAC caused hepatic damage. Hindawi Publishing Corporation 2016 2016-11-13 /pmc/articles/PMC5124475/ /pubmed/27957238 http://dx.doi.org/10.1155/2016/4047362 Text en Copyright © 2016 Fabiana Andréa Moura et al. https://creativecommons.org/licenses/by/4.0/ 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
Moura, Fabiana Andréa
de Andrade, Kívia Queiroz
de Araújo, Orlando Roberto Pimentel
Nunes-Souza, Valéria
Santos, Juliana Célia de Farias
Rabelo, Luiza Antas
Goulart, Marília Oliveira Fonseca
Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title_full Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title_fullStr Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title_full_unstemmed Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title_short Colonic and Hepatic Modulation by Lipoic Acid and/or N-Acetylcysteine Supplementation in Mild Ulcerative Colitis Induced by Dextran Sodium Sulfate in Rats
title_sort colonic and hepatic modulation by lipoic acid and/or n-acetylcysteine supplementation in mild ulcerative colitis induced by dextran sodium sulfate in rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124475/
https://www.ncbi.nlm.nih.gov/pubmed/27957238
http://dx.doi.org/10.1155/2016/4047362
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