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Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway
Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were ora...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463179/ https://www.ncbi.nlm.nih.gov/pubmed/34567209 http://dx.doi.org/10.1155/2021/3334994 |
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author | Kang, Zeng-Ping Wang, Meng-Xue Wu, Tian-Tian Liu, Duan-Yong Wang, Hai-Yan Long, Jian Zhao, Hai-Mei Zhong, You-Bao |
author_facet | Kang, Zeng-Ping Wang, Meng-Xue Wu, Tian-Tian Liu, Duan-Yong Wang, Hai-Yan Long, Jian Zhao, Hai-Mei Zhong, You-Bao |
author_sort | Kang, Zeng-Ping |
collection | PubMed |
description | Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1β, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11b(+)F4/80(+) and CD11b(+)F4/80(+)TIM-1(+) and CD11b(+)F4/80(+)iNOS(+) decreased significantly and CD11b(+)F4/80(+)CD206(+) and CD11b(+)F4/80(+)CD163(+) increased significantly. Additionally, curcumin significantly downregulated CD11b(+)F4/80(+)TLR4(+) macrophages and the protein levels of TLR2, TLR4, MyD88, NF-κBp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway. |
format | Online Article Text |
id | pubmed-8463179 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-84631792021-09-25 Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway Kang, Zeng-Ping Wang, Meng-Xue Wu, Tian-Tian Liu, Duan-Yong Wang, Hai-Yan Long, Jian Zhao, Hai-Mei Zhong, You-Bao Evid Based Complement Alternat Med Research Article Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1β, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11b(+)F4/80(+) and CD11b(+)F4/80(+)TIM-1(+) and CD11b(+)F4/80(+)iNOS(+) decreased significantly and CD11b(+)F4/80(+)CD206(+) and CD11b(+)F4/80(+)CD163(+) increased significantly. Additionally, curcumin significantly downregulated CD11b(+)F4/80(+)TLR4(+) macrophages and the protein levels of TLR2, TLR4, MyD88, NF-κBp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway. Hindawi 2021-09-16 /pmc/articles/PMC8463179/ /pubmed/34567209 http://dx.doi.org/10.1155/2021/3334994 Text en Copyright © 2021 Zeng-Ping Kang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Kang, Zeng-Ping Wang, Meng-Xue Wu, Tian-Tian Liu, Duan-Yong Wang, Hai-Yan Long, Jian Zhao, Hai-Mei Zhong, You-Bao Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title | Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title_full | Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title_fullStr | Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title_full_unstemmed | Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title_short | Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway |
title_sort | curcumin alleviated dextran sulfate sodium-induced colitis by regulating m1/m2 macrophage polarization and tlrs signaling pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463179/ https://www.ncbi.nlm.nih.gov/pubmed/34567209 http://dx.doi.org/10.1155/2021/3334994 |
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