Cargando…
Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models
Background. This study was pathway of (−)-epicatechin (EC) in the prevention and treatment of intestine inflammation in acute and chronic rat models. Methods. Intestine inflammation was induced in rats using TNBS. The morphological, inflammatory, immunohistochemical, and immunoblotting characteristi...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546492/ https://www.ncbi.nlm.nih.gov/pubmed/23346204 http://dx.doi.org/10.1155/2012/508902 |
_version_ | 1782256066443083776 |
---|---|
author | Vasconcelos, Paulo César de Paula Seito, Leonardo Noboru Di Stasi, Luiz Cláudio Akiko Hiruma-Lima, Clélia Pellizzon, Cláudia Helena |
author_facet | Vasconcelos, Paulo César de Paula Seito, Leonardo Noboru Di Stasi, Luiz Cláudio Akiko Hiruma-Lima, Clélia Pellizzon, Cláudia Helena |
author_sort | Vasconcelos, Paulo César de Paula |
collection | PubMed |
description | Background. This study was pathway of (−)-epicatechin (EC) in the prevention and treatment of intestine inflammation in acute and chronic rat models. Methods. Intestine inflammation was induced in rats using TNBS. The morphological, inflammatory, immunohistochemical, and immunoblotting characteristics of colon samples were examined. The effects of EC were evaluated in an acute model at doses of 5, 10, 25, and 50 mg/kg by gavage for 5 days. The chronic colitis model was induced 1st day, and treated for 21 days. For the colitis relapse model, the induction was repeated on 14th. Results. EC10 and EC50 effectively reduced the lesion size, as assessed macroscopically; and confirmed by microscopy for EC10. The glutathione levels were higher in EC10 group but decreased COX-2 expression and increased cell proliferation (PC) were observed, indicating an anti-inflammatory activity and a proliferation-stimulating effect. In the chronic colitis model, EC10 showed lower macroscopic and microscopic lesion scores and increase in glutathione levels. As in the acute model, a decrease in COX-2 expression and an increase in PC in EC10, the chronic model this increase maybe by the pathway EGF expression. Conclusion. These results confirm the activity of EC as an antioxidant that reduces of the lesion and that has the potential to stimulate tissue healing, indicating useful for preventing and treating intestine inflammation. |
format | Online Article Text |
id | pubmed-3546492 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-35464922013-01-23 Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models Vasconcelos, Paulo César de Paula Seito, Leonardo Noboru Di Stasi, Luiz Cláudio Akiko Hiruma-Lima, Clélia Pellizzon, Cláudia Helena Evid Based Complement Alternat Med Research Article Background. This study was pathway of (−)-epicatechin (EC) in the prevention and treatment of intestine inflammation in acute and chronic rat models. Methods. Intestine inflammation was induced in rats using TNBS. The morphological, inflammatory, immunohistochemical, and immunoblotting characteristics of colon samples were examined. The effects of EC were evaluated in an acute model at doses of 5, 10, 25, and 50 mg/kg by gavage for 5 days. The chronic colitis model was induced 1st day, and treated for 21 days. For the colitis relapse model, the induction was repeated on 14th. Results. EC10 and EC50 effectively reduced the lesion size, as assessed macroscopically; and confirmed by microscopy for EC10. The glutathione levels were higher in EC10 group but decreased COX-2 expression and increased cell proliferation (PC) were observed, indicating an anti-inflammatory activity and a proliferation-stimulating effect. In the chronic colitis model, EC10 showed lower macroscopic and microscopic lesion scores and increase in glutathione levels. As in the acute model, a decrease in COX-2 expression and an increase in PC in EC10, the chronic model this increase maybe by the pathway EGF expression. Conclusion. These results confirm the activity of EC as an antioxidant that reduces of the lesion and that has the potential to stimulate tissue healing, indicating useful for preventing and treating intestine inflammation. Hindawi Publishing Corporation 2012 2012-12-30 /pmc/articles/PMC3546492/ /pubmed/23346204 http://dx.doi.org/10.1155/2012/508902 Text en Copyright © 2012 Paulo César de Paula Vasconcelos et al. https://creativecommons.org/licenses/by/3.0/ 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 Vasconcelos, Paulo César de Paula Seito, Leonardo Noboru Di Stasi, Luiz Cláudio Akiko Hiruma-Lima, Clélia Pellizzon, Cláudia Helena Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title | Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title_full | Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title_fullStr | Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title_full_unstemmed | Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title_short | Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models |
title_sort | epicatechin used in the treatment of intestinal inflammatory disease: an analysis by experimental models |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546492/ https://www.ncbi.nlm.nih.gov/pubmed/23346204 http://dx.doi.org/10.1155/2012/508902 |
work_keys_str_mv | AT vasconcelospaulocesardepaula epicatechinusedinthetreatmentofintestinalinflammatorydiseaseananalysisbyexperimentalmodels AT seitoleonardonoboru epicatechinusedinthetreatmentofintestinalinflammatorydiseaseananalysisbyexperimentalmodels AT distasiluizclaudio epicatechinusedinthetreatmentofintestinalinflammatorydiseaseananalysisbyexperimentalmodels AT akikohirumalimaclelia epicatechinusedinthetreatmentofintestinalinflammatorydiseaseananalysisbyexperimentalmodels AT pellizzonclaudiahelena epicatechinusedinthetreatmentofintestinalinflammatorydiseaseananalysisbyexperimentalmodels |