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Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice

BACKGROUND/AIMS: Inflammatory bowel disease (IBD) is an autoimmune disease characterized by chronic inflammation mainly in the large intestine. The interleukin-10 knockout (IL-10 KO) mouse is a well-known animal model of IBD that develops spontaneous intestinal inflammation resembling Crohn’s diseas...

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Autores principales: Jung, Kyong Jin, Lee, Gun Woo, Park, Chul Hyun, Lee, Tae Jin, Kim, Joo Young, Sung, Eon Gi, Kim, Seong Yong, Jang, Byung Ik, Song, In Hwan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Editorial Office of Gut and Liver 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974321/
https://www.ncbi.nlm.nih.gov/pubmed/31158947
http://dx.doi.org/10.5009/gnl18438
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author Jung, Kyong Jin
Lee, Gun Woo
Park, Chul Hyun
Lee, Tae Jin
Kim, Joo Young
Sung, Eon Gi
Kim, Seong Yong
Jang, Byung Ik
Song, In Hwan
author_facet Jung, Kyong Jin
Lee, Gun Woo
Park, Chul Hyun
Lee, Tae Jin
Kim, Joo Young
Sung, Eon Gi
Kim, Seong Yong
Jang, Byung Ik
Song, In Hwan
author_sort Jung, Kyong Jin
collection PubMed
description BACKGROUND/AIMS: Inflammatory bowel disease (IBD) is an autoimmune disease characterized by chronic inflammation mainly in the large intestine. The interleukin-10 knockout (IL-10 KO) mouse is a well-known animal model of IBD that develops spontaneous intestinal inflammation resembling Crohn’s disease. Oxidative stress is considered to be the leading cause of cell and tissue damage. Reactive oxygen species (ROS) can cause direct cell injury and/or indirect cell injury by inducing the secretion of cytokines from damaged cells. This study evaluated the effects of mesenchymal stem cell (MSC) on the progression of IBD. METHODS: In this study, human bone marrow-derived MSCs were injected into IL-10 KO mice (MSC). Oxidative stress and inflammation levels were evaluated in the large intestine and compared with those in control IL-10 KO mice (CON) and normal wild-type control mice (Wild). RESULTS: The levels of ROS (superoxide and hydrogen peroxidase) and a secondary end-product of lipid peroxidation (malondialdehyde) were considerably higher in the CON, while superoxide dismutase and catalase levels were lower in the MSC. Inflammation-related marker (interferon-γ, tumor necrosis factor-α, IL-4, and CD8) expression and inflammatory histological changes were much less pronounced in MSC than in CON. CONCLUSIONS: MSCs affect the redox balance, leading to the suppression of IBD.
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spelling pubmed-69743212020-02-03 Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice Jung, Kyong Jin Lee, Gun Woo Park, Chul Hyun Lee, Tae Jin Kim, Joo Young Sung, Eon Gi Kim, Seong Yong Jang, Byung Ik Song, In Hwan Gut Liver Original Article BACKGROUND/AIMS: Inflammatory bowel disease (IBD) is an autoimmune disease characterized by chronic inflammation mainly in the large intestine. The interleukin-10 knockout (IL-10 KO) mouse is a well-known animal model of IBD that develops spontaneous intestinal inflammation resembling Crohn’s disease. Oxidative stress is considered to be the leading cause of cell and tissue damage. Reactive oxygen species (ROS) can cause direct cell injury and/or indirect cell injury by inducing the secretion of cytokines from damaged cells. This study evaluated the effects of mesenchymal stem cell (MSC) on the progression of IBD. METHODS: In this study, human bone marrow-derived MSCs were injected into IL-10 KO mice (MSC). Oxidative stress and inflammation levels were evaluated in the large intestine and compared with those in control IL-10 KO mice (CON) and normal wild-type control mice (Wild). RESULTS: The levels of ROS (superoxide and hydrogen peroxidase) and a secondary end-product of lipid peroxidation (malondialdehyde) were considerably higher in the CON, while superoxide dismutase and catalase levels were lower in the MSC. Inflammation-related marker (interferon-γ, tumor necrosis factor-α, IL-4, and CD8) expression and inflammatory histological changes were much less pronounced in MSC than in CON. CONCLUSIONS: MSCs affect the redox balance, leading to the suppression of IBD. Editorial Office of Gut and Liver 2020-01 2019-09-19 /pmc/articles/PMC6974321/ /pubmed/31158947 http://dx.doi.org/10.5009/gnl18438 Text en Copyright © 2020 by The Korean Society of Gastroenterology, the Korean Society of Gastrointestinal Endoscopy, the Korean Society of Neurogastroenterology and Motility, Korean College of Helicobacter and Upper Gastrointestinal Research, Korean Association the Study of Intestinal Diseases, the Korean Association for the Study of the Liver, Korean Pancreatobiliary Association, and Korean Society of Gastrointestinal Cancer. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Jung, Kyong Jin
Lee, Gun Woo
Park, Chul Hyun
Lee, Tae Jin
Kim, Joo Young
Sung, Eon Gi
Kim, Seong Yong
Jang, Byung Ik
Song, In Hwan
Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title_full Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title_fullStr Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title_full_unstemmed Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title_short Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice
title_sort mesenchymal stem cells decrease oxidative stress in the bowels of interleukin-10 knockout mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974321/
https://www.ncbi.nlm.nih.gov/pubmed/31158947
http://dx.doi.org/10.5009/gnl18438
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