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The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells

Background and objectives: Non-steroidal anti-inflammatory drugs (NSAIDs) have been among the major causes of small intestinal injury in clinical practice. As such, the current study investigated the protective effect of 5-aminosalicylic acid (5-ASA) against an NSAID-induced small intestinal injury....

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Autores principales: Jung, Eun Suk, Jang, Hyun Joo, Hong, Eun Mi, Lim, Hye Li, Lee, Sang Pyo, Kae, Sea Hyub, Lee, Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600857/
https://www.ncbi.nlm.nih.gov/pubmed/33019698
http://dx.doi.org/10.3390/medicina56100515
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author Jung, Eun Suk
Jang, Hyun Joo
Hong, Eun Mi
Lim, Hye Li
Lee, Sang Pyo
Kae, Sea Hyub
Lee, Jin
author_facet Jung, Eun Suk
Jang, Hyun Joo
Hong, Eun Mi
Lim, Hye Li
Lee, Sang Pyo
Kae, Sea Hyub
Lee, Jin
author_sort Jung, Eun Suk
collection PubMed
description Background and objectives: Non-steroidal anti-inflammatory drugs (NSAIDs) have been among the major causes of small intestinal injury in clinical practice. As such, the current study investigated the protective effect of 5-aminosalicylic acid (5-ASA) against an NSAID-induced small intestinal injury. Materials and Methods: IEC-6 cells were treated with various concentrations of indomethacin with or without 5-ASA in a serum-free medium, after which an 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Dromide (MTT) assay, a cell apoptosis assay, a caspase-3 activity assay, a reactive oxygen species (ROS) content and Superoxide dismutase 2 (SOD2) activity measurement, a Western blotting for occludin and zonula occludens-1 (ZO-1) and a wound healing assay were conducted. Results: 5-ASA ameliorated indomethacin-induced cell apoptosis and an increase in the intracellular ROS content while augmenting the indomethacin-induced suppression of SOD2 activity in IEC-6 cells. Moreover, 5-ASA reversed the indomethacin-induced attenuation of occludin and ZO-1 expression and promoted faster wound healing effects in IEC-6 cells following an indomethacin-induced injury. Conclusions: Our results suggested that 5-ASA protects small intestinal cells against an NSAID-induced small intestinal injury by scavenging free radicals. Therefore, 5-ASA could be a potential treatment for an NSAID-induced small intestinal injury.
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spelling pubmed-76008572020-11-01 The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells Jung, Eun Suk Jang, Hyun Joo Hong, Eun Mi Lim, Hye Li Lee, Sang Pyo Kae, Sea Hyub Lee, Jin Medicina (Kaunas) Article Background and objectives: Non-steroidal anti-inflammatory drugs (NSAIDs) have been among the major causes of small intestinal injury in clinical practice. As such, the current study investigated the protective effect of 5-aminosalicylic acid (5-ASA) against an NSAID-induced small intestinal injury. Materials and Methods: IEC-6 cells were treated with various concentrations of indomethacin with or without 5-ASA in a serum-free medium, after which an 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Dromide (MTT) assay, a cell apoptosis assay, a caspase-3 activity assay, a reactive oxygen species (ROS) content and Superoxide dismutase 2 (SOD2) activity measurement, a Western blotting for occludin and zonula occludens-1 (ZO-1) and a wound healing assay were conducted. Results: 5-ASA ameliorated indomethacin-induced cell apoptosis and an increase in the intracellular ROS content while augmenting the indomethacin-induced suppression of SOD2 activity in IEC-6 cells. Moreover, 5-ASA reversed the indomethacin-induced attenuation of occludin and ZO-1 expression and promoted faster wound healing effects in IEC-6 cells following an indomethacin-induced injury. Conclusions: Our results suggested that 5-ASA protects small intestinal cells against an NSAID-induced small intestinal injury by scavenging free radicals. Therefore, 5-ASA could be a potential treatment for an NSAID-induced small intestinal injury. MDPI 2020-10-01 /pmc/articles/PMC7600857/ /pubmed/33019698 http://dx.doi.org/10.3390/medicina56100515 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Jung, Eun Suk
Jang, Hyun Joo
Hong, Eun Mi
Lim, Hye Li
Lee, Sang Pyo
Kae, Sea Hyub
Lee, Jin
The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title_full The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title_fullStr The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title_full_unstemmed The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title_short The Protective Effect of 5-Aminosalicylic Acid against Non-Steroidal Anti-Inflammatory Drug-Induced Injury through Free Radical Scavenging in Small Intestinal Epithelial Cells
title_sort protective effect of 5-aminosalicylic acid against non-steroidal anti-inflammatory drug-induced injury through free radical scavenging in small intestinal epithelial cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600857/
https://www.ncbi.nlm.nih.gov/pubmed/33019698
http://dx.doi.org/10.3390/medicina56100515
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