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Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice
Reactive oxygen species (ROS), which are exceptionally high in IBD lesions, are known to cause abnormal immune responses to inflammatory reactions in inflammatory bowel diseases (IBD) through damage to the intestinal mucosal linings. Moreover, they are theorized to be an agent of IBD development. Vi...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9505994/ https://www.ncbi.nlm.nih.gov/pubmed/36142515 http://dx.doi.org/10.3390/ijms231810612 |
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author | Jo, Hyejung Lee, Dahae Go, Cheolhyeon Jang, Yoojin Chu, Naghyung Bae, Suhyun Kang, Dongmin Im, Jong Pil Kim, Yejin Kang, Jae Seung |
author_facet | Jo, Hyejung Lee, Dahae Go, Cheolhyeon Jang, Yoojin Chu, Naghyung Bae, Suhyun Kang, Dongmin Im, Jong Pil Kim, Yejin Kang, Jae Seung |
author_sort | Jo, Hyejung |
collection | PubMed |
description | Reactive oxygen species (ROS), which are exceptionally high in IBD lesions, are known to cause abnormal immune responses to inflammatory reactions in inflammatory bowel diseases (IBD) through damage to the intestinal mucosal linings. Moreover, they are theorized to be an agent of IBD development. Vitamin C is widely known to be an effective antioxidant for its ability to regulate inflammatory responses through its ROS scavenging effect. Therefore, we examined vitamin C’s influence on the development and progression of IBD in Gulo(−/−) mice, which cannot synthesize vitamin C like humans due to a defect in the expression of L-gulono-γ–lactone oxidase, an essential enzyme for vitamin C production. First, we found extensive oxidative stress and an inflammation increase in the colon of vitamin C-insufficient Gulo(−/−) mice. We also found decreased IL-22 production and NKp46(+) cell recruitment and the impaired activation of the p38MAPK pathway. Additionally, comparing vitamin C-insufficient Gulo(−/−) mice to vitamin C-sufficient Gulo(−/−) mice and wild-type mice, the insufficient group faced a decrease in mucin-1 expression, accompanied by an increase in IL-6 production, followed by the activation of the STAT3 and Akt pathways. The results suggest that vitamin C insufficiency induces severe colitis, meaning vitamin C could also take on a preventative role by regulating the production of cytokines and the induction of inflammation. |
format | Online Article Text |
id | pubmed-9505994 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95059942022-09-24 Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice Jo, Hyejung Lee, Dahae Go, Cheolhyeon Jang, Yoojin Chu, Naghyung Bae, Suhyun Kang, Dongmin Im, Jong Pil Kim, Yejin Kang, Jae Seung Int J Mol Sci Article Reactive oxygen species (ROS), which are exceptionally high in IBD lesions, are known to cause abnormal immune responses to inflammatory reactions in inflammatory bowel diseases (IBD) through damage to the intestinal mucosal linings. Moreover, they are theorized to be an agent of IBD development. Vitamin C is widely known to be an effective antioxidant for its ability to regulate inflammatory responses through its ROS scavenging effect. Therefore, we examined vitamin C’s influence on the development and progression of IBD in Gulo(−/−) mice, which cannot synthesize vitamin C like humans due to a defect in the expression of L-gulono-γ–lactone oxidase, an essential enzyme for vitamin C production. First, we found extensive oxidative stress and an inflammation increase in the colon of vitamin C-insufficient Gulo(−/−) mice. We also found decreased IL-22 production and NKp46(+) cell recruitment and the impaired activation of the p38MAPK pathway. Additionally, comparing vitamin C-insufficient Gulo(−/−) mice to vitamin C-sufficient Gulo(−/−) mice and wild-type mice, the insufficient group faced a decrease in mucin-1 expression, accompanied by an increase in IL-6 production, followed by the activation of the STAT3 and Akt pathways. The results suggest that vitamin C insufficiency induces severe colitis, meaning vitamin C could also take on a preventative role by regulating the production of cytokines and the induction of inflammation. MDPI 2022-09-13 /pmc/articles/PMC9505994/ /pubmed/36142515 http://dx.doi.org/10.3390/ijms231810612 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Jo, Hyejung Lee, Dahae Go, Cheolhyeon Jang, Yoojin Chu, Naghyung Bae, Suhyun Kang, Dongmin Im, Jong Pil Kim, Yejin Kang, Jae Seung Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title | Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title_full | Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title_fullStr | Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title_full_unstemmed | Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title_short | Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(−/−) Mice |
title_sort | preventive effect of vitamin c on dextran sulfate sodium (dss)-induced colitis via the regulation of il-22 and il-6 production in gulo(−/−) mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9505994/ https://www.ncbi.nlm.nih.gov/pubmed/36142515 http://dx.doi.org/10.3390/ijms231810612 |
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