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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...

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Autores principales: Jo, Hyejung, Lee, Dahae, Go, Cheolhyeon, Jang, Yoojin, Chu, Naghyung, Bae, Suhyun, Kang, Dongmin, Im, Jong Pil, Kim, Yejin, Kang, Jae Seung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
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.
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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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