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Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis
Astaxanthin is a xanthophyll carotenoid, which possesses strong scavenging effect on reactive oxygen species. In this study, we examined the effect of astaxanthin on dextran sulfate sodium (DSS)-induced colitis in mice. Experimental colitis was induced by the oral administration of 4% w/v DSS in tap...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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the Society for Free Radical Research Japan
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348411/ https://www.ncbi.nlm.nih.gov/pubmed/30705514 http://dx.doi.org/10.3164/jcbn.18-47 |
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author | Sakai, Shigeki Nishida, Atsushi Ohno, Masashi Inatomi, Osamu Bamba, Shigeki Sugimoto, Mitsushige Kawahara, Masahiro Andoh, Akira |
author_facet | Sakai, Shigeki Nishida, Atsushi Ohno, Masashi Inatomi, Osamu Bamba, Shigeki Sugimoto, Mitsushige Kawahara, Masahiro Andoh, Akira |
author_sort | Sakai, Shigeki |
collection | PubMed |
description | Astaxanthin is a xanthophyll carotenoid, which possesses strong scavenging effect on reactive oxygen species. In this study, we examined the effect of astaxanthin on dextran sulfate sodium (DSS)-induced colitis in mice. Experimental colitis was induced by the oral administration of 4% w/v DSS in tap water in C57BL/6J mice. Astaxanthin was mixed with a normal rodent diet (0.02 or 0.04%). Astaxanthin significantly ameliorated DSS-induced body weight loss and reduced the disease activity index. The ameliorating effects was observed in a dose-dependent manner. Immunochemical analyses showed that astaxanthin markedly suppressed DSS-induced histological inflammatory changes (inflammatory cell infiltration, edematous changes and goblet cell depletion). Plasma levels of malondialdehyde and 8-hydroxy-2-deoxyguanosine were significantly reduced by the administration of 0.04% astaxanthin. Astaxanthin significantly suppressed the mucosal mRNA expression of IL-1β, IL-6, TNF-α, IL-36α and IL-36γ. Astaxanthin blocked the DSS-induced translocation of NF-κB p65 and AP-1 (c-Jun) into the nucleus of mucosal epithelial cells, and also suppressed DSS-induced mucosal activation of MAPKs (ERK1/2, p38 and JNK). In conclusion, astaxanthin prevented the development of DSS-induced colitis via the direct suppression of NF-κB, AP-1 and MAPK activation. These findings suggest that astaxanthin is a novel candidate as a therapeutic option for the treatment of inflammatory bowel disease. |
format | Online Article Text |
id | pubmed-6348411 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | the Society for Free Radical Research Japan |
record_format | MEDLINE/PubMed |
spelling | pubmed-63484112019-01-31 Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis Sakai, Shigeki Nishida, Atsushi Ohno, Masashi Inatomi, Osamu Bamba, Shigeki Sugimoto, Mitsushige Kawahara, Masahiro Andoh, Akira J Clin Biochem Nutr Original Article Astaxanthin is a xanthophyll carotenoid, which possesses strong scavenging effect on reactive oxygen species. In this study, we examined the effect of astaxanthin on dextran sulfate sodium (DSS)-induced colitis in mice. Experimental colitis was induced by the oral administration of 4% w/v DSS in tap water in C57BL/6J mice. Astaxanthin was mixed with a normal rodent diet (0.02 or 0.04%). Astaxanthin significantly ameliorated DSS-induced body weight loss and reduced the disease activity index. The ameliorating effects was observed in a dose-dependent manner. Immunochemical analyses showed that astaxanthin markedly suppressed DSS-induced histological inflammatory changes (inflammatory cell infiltration, edematous changes and goblet cell depletion). Plasma levels of malondialdehyde and 8-hydroxy-2-deoxyguanosine were significantly reduced by the administration of 0.04% astaxanthin. Astaxanthin significantly suppressed the mucosal mRNA expression of IL-1β, IL-6, TNF-α, IL-36α and IL-36γ. Astaxanthin blocked the DSS-induced translocation of NF-κB p65 and AP-1 (c-Jun) into the nucleus of mucosal epithelial cells, and also suppressed DSS-induced mucosal activation of MAPKs (ERK1/2, p38 and JNK). In conclusion, astaxanthin prevented the development of DSS-induced colitis via the direct suppression of NF-κB, AP-1 and MAPK activation. These findings suggest that astaxanthin is a novel candidate as a therapeutic option for the treatment of inflammatory bowel disease. the Society for Free Radical Research Japan 2019-01 2018-08-11 /pmc/articles/PMC6348411/ /pubmed/30705514 http://dx.doi.org/10.3164/jcbn.18-47 Text en Copyright © 2019 JCBN http://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Sakai, Shigeki Nishida, Atsushi Ohno, Masashi Inatomi, Osamu Bamba, Shigeki Sugimoto, Mitsushige Kawahara, Masahiro Andoh, Akira Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title | Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title_full | Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title_fullStr | Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title_full_unstemmed | Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title_short | Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
title_sort | astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348411/ https://www.ncbi.nlm.nih.gov/pubmed/30705514 http://dx.doi.org/10.3164/jcbn.18-47 |
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