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Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice
Curcumin and resveratrol are two natural products, which have been described as potential anti-inflammatory, anti-tumor, and anti-oxidant molecules. The aims of the present study were to investigate the protective effect of curcumin and resveratrol on dextran sulfate sodium (DSS)-induced ulcerative...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423642/ https://www.ncbi.nlm.nih.gov/pubmed/30816479 http://dx.doi.org/10.3892/mmr.2019.9974 |
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author | Zhang, Lize Xue, Hui Zhao, Gang Qiao, Cuixia Sun, Xiaomei Pang, Chengjian Zhang, Dianliang |
author_facet | Zhang, Lize Xue, Hui Zhao, Gang Qiao, Cuixia Sun, Xiaomei Pang, Chengjian Zhang, Dianliang |
author_sort | Zhang, Lize |
collection | PubMed |
description | Curcumin and resveratrol are two natural products, which have been described as potential anti-inflammatory, anti-tumor, and anti-oxidant molecules. The aims of the present study were to investigate the protective effect of curcumin and resveratrol on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice, in addition to understanding the underlying molecular mechanisms. In order to accomplish this, BALB/c mice received drinking water containing 3.5% DSS. Curcumin (50 mg/kg/day) or resveratrol (80 mg/kg/day) were administered orally for 7 days. Survival rate, body weight, disease activity index score, colon length, pro-inflammatory cytokines, and the expression autophagy-associated proteins, and mechanistic target of rapamycin (mTOR) and sirtuin 1 (SIRT1) were measured. Curcumin or resveratrol treatment prolonged the survival of mice with UC, reduced body weight loss and attenuated the severity of the disease compared with the DSS-treated mice. This effect was associated with a substantial clinical amelioration of the disruption of the colonic architecture and a significant reduction in pro-inflammatory cytokine production. Furthermore, curcumin or resveratrol significantly downregulated the expression of autophagy-related 12, Beclin-1 and microtubule-associated protein light chain 3 II, and upregulated the expression of phosphorylated mTOR and SIRT1 in the colon tissue, compared with those in the DSS-treated group. These results suggest that curcumin and resveratrol exert protective effects on DSS-induced UC, partially through suppressing the intestinal inflammatory cascade reaction, reducing autophagy and regulating SIRT1/mTOR signaling. |
format | Online Article Text |
id | pubmed-6423642 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-64236422019-03-22 Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice Zhang, Lize Xue, Hui Zhao, Gang Qiao, Cuixia Sun, Xiaomei Pang, Chengjian Zhang, Dianliang Mol Med Rep Articles Curcumin and resveratrol are two natural products, which have been described as potential anti-inflammatory, anti-tumor, and anti-oxidant molecules. The aims of the present study were to investigate the protective effect of curcumin and resveratrol on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice, in addition to understanding the underlying molecular mechanisms. In order to accomplish this, BALB/c mice received drinking water containing 3.5% DSS. Curcumin (50 mg/kg/day) or resveratrol (80 mg/kg/day) were administered orally for 7 days. Survival rate, body weight, disease activity index score, colon length, pro-inflammatory cytokines, and the expression autophagy-associated proteins, and mechanistic target of rapamycin (mTOR) and sirtuin 1 (SIRT1) were measured. Curcumin or resveratrol treatment prolonged the survival of mice with UC, reduced body weight loss and attenuated the severity of the disease compared with the DSS-treated mice. This effect was associated with a substantial clinical amelioration of the disruption of the colonic architecture and a significant reduction in pro-inflammatory cytokine production. Furthermore, curcumin or resveratrol significantly downregulated the expression of autophagy-related 12, Beclin-1 and microtubule-associated protein light chain 3 II, and upregulated the expression of phosphorylated mTOR and SIRT1 in the colon tissue, compared with those in the DSS-treated group. These results suggest that curcumin and resveratrol exert protective effects on DSS-induced UC, partially through suppressing the intestinal inflammatory cascade reaction, reducing autophagy and regulating SIRT1/mTOR signaling. D.A. Spandidos 2019-04 2019-02-20 /pmc/articles/PMC6423642/ /pubmed/30816479 http://dx.doi.org/10.3892/mmr.2019.9974 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhang, Lize Xue, Hui Zhao, Gang Qiao, Cuixia Sun, Xiaomei Pang, Chengjian Zhang, Dianliang Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title | Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title_full | Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title_fullStr | Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title_full_unstemmed | Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title_short | Curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
title_sort | curcumin and resveratrol suppress dextran sulfate sodium-induced colitis in mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423642/ https://www.ncbi.nlm.nih.gov/pubmed/30816479 http://dx.doi.org/10.3892/mmr.2019.9974 |
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