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Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells
AIM: To verify whether curcumin (Cur) can treat inflammatory bowel disease by regulating CD8(+)CD11c(+) cells. METHODS: We evaluated the suppressive effect of Cur on CD8(+)CD11c(+) cells in spleen and Peyer’s patches (PPs) in colitis induced by trinitrobenzene sulfonic acid. Mice with colitis were t...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5352921/ https://www.ncbi.nlm.nih.gov/pubmed/28348486 http://dx.doi.org/10.3748/wjg.v23.i10.1804 |
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author | Zhao, Hai-Mei Han, Fei Xu, Rong Huang, Xiao-Ying Cheng, Shao-Min Huang, Min-Fang Yue, Hai-Yang Wang, Xin Zou, Yong Xu, Han-Lin Liu, Duan-Yong |
author_facet | Zhao, Hai-Mei Han, Fei Xu, Rong Huang, Xiao-Ying Cheng, Shao-Min Huang, Min-Fang Yue, Hai-Yang Wang, Xin Zou, Yong Xu, Han-Lin Liu, Duan-Yong |
author_sort | Zhao, Hai-Mei |
collection | PubMed |
description | AIM: To verify whether curcumin (Cur) can treat inflammatory bowel disease by regulating CD8(+)CD11c(+) cells. METHODS: We evaluated the suppressive effect of Cur on CD8(+)CD11c(+) cells in spleen and Peyer’s patches (PPs) in colitis induced by trinitrobenzene sulfonic acid. Mice with colitis were treated by 200 mg/kg Cur for 7 d. On day 8, the therapeutic effect of Cur was evaluated by visual assessment and histological examination, while co-stimulatory molecules of CD8(+)CD11c(+) cells in the spleen and PPs were measured by flow cytometry. The levels of interleukin (IL)-10, interferon (IFN)-γ and transforming growth factor (TGF)-β1 in spleen and colonic mucosa were determined by ELISA. RESULTS: The disease activity index, colon weight, weight index of colon and histological score of experimental colitis were obviously decreased after Cur treatment, while the body weight and colon length recovered. After treatment with Cur, CD8(+)CD11c(+) cells were decreased in the spleen and PPs, and the expression of major histocompatibility complex II, CD205, CD40, CD40L and intercellular adhesion molecule-1 was inhibited. IL-10, IFN-γ and TGF-β1 levels were increased compared with those in mice with untreated colitis. CONCLUSION: Cur can effectively treat experimental colitis, which is realized by inhibiting CD8(+)CD11c(+) cells. |
format | Online Article Text |
id | pubmed-5352921 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-53529212017-03-27 Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells Zhao, Hai-Mei Han, Fei Xu, Rong Huang, Xiao-Ying Cheng, Shao-Min Huang, Min-Fang Yue, Hai-Yang Wang, Xin Zou, Yong Xu, Han-Lin Liu, Duan-Yong World J Gastroenterol Basic Study AIM: To verify whether curcumin (Cur) can treat inflammatory bowel disease by regulating CD8(+)CD11c(+) cells. METHODS: We evaluated the suppressive effect of Cur on CD8(+)CD11c(+) cells in spleen and Peyer’s patches (PPs) in colitis induced by trinitrobenzene sulfonic acid. Mice with colitis were treated by 200 mg/kg Cur for 7 d. On day 8, the therapeutic effect of Cur was evaluated by visual assessment and histological examination, while co-stimulatory molecules of CD8(+)CD11c(+) cells in the spleen and PPs were measured by flow cytometry. The levels of interleukin (IL)-10, interferon (IFN)-γ and transforming growth factor (TGF)-β1 in spleen and colonic mucosa were determined by ELISA. RESULTS: The disease activity index, colon weight, weight index of colon and histological score of experimental colitis were obviously decreased after Cur treatment, while the body weight and colon length recovered. After treatment with Cur, CD8(+)CD11c(+) cells were decreased in the spleen and PPs, and the expression of major histocompatibility complex II, CD205, CD40, CD40L and intercellular adhesion molecule-1 was inhibited. IL-10, IFN-γ and TGF-β1 levels were increased compared with those in mice with untreated colitis. CONCLUSION: Cur can effectively treat experimental colitis, which is realized by inhibiting CD8(+)CD11c(+) cells. Baishideng Publishing Group Inc 2017-03-14 2017-03-14 /pmc/articles/PMC5352921/ /pubmed/28348486 http://dx.doi.org/10.3748/wjg.v23.i10.1804 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Basic Study Zhao, Hai-Mei Han, Fei Xu, Rong Huang, Xiao-Ying Cheng, Shao-Min Huang, Min-Fang Yue, Hai-Yang Wang, Xin Zou, Yong Xu, Han-Lin Liu, Duan-Yong Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title | Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title_full | Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title_fullStr | Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title_full_unstemmed | Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title_short | Therapeutic effect of curcumin on experimental colitis mediated by inhibiting CD8(+)CD11c(+) cells |
title_sort | therapeutic effect of curcumin on experimental colitis mediated by inhibiting cd8(+)cd11c(+) cells |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5352921/ https://www.ncbi.nlm.nih.gov/pubmed/28348486 http://dx.doi.org/10.3748/wjg.v23.i10.1804 |
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