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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/75327
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dc.contributor.authorWitaicenis, Aline-
dc.contributor.authorLuchini, A. C.-
dc.contributor.authorHiruma-Lima, C. A.-
dc.contributor.authorFelisbino, S. L.-
dc.contributor.authorJustulin, L. A.-
dc.contributor.authorGarrido-Mesa, N.-
dc.contributor.authorUtrilla, P.-
dc.contributor.authorGálvez, J.-
dc.contributor.authorDi Stasi, L. C.-
dc.date.accessioned2014-05-27T11:29:05Z-
dc.date.accessioned2016-10-25T18:48:14Z-
dc.date.available2014-05-27T11:29:05Z-
dc.date.available2016-10-25T18:48:14Z-
dc.date.issued2013-05-01-
dc.identifierhttp://www.biolifesas.org/ejoi/abstractsEJI11-2.pdf-
dc.identifier.citationEuropean Journal of Inflammation, v. 11, n. 2, p. 433-446, 2013.-
dc.identifier.issn1721-727X-
dc.identifier.urihttp://hdl.handle.net/11449/75327-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/75327-
dc.description.abstractEsculetin is a coumarin derivative with high antioxidant activity. In a rat experimental model of inflammatory bowel disease induced by trinitrobenzenesulfonic acid, esculetin at the dose of 5mg/Kg displayed intestinal anti-inflammatory activity; however, its mechanism of action needs to be elucidated. Our objective was to evaluate the effects of esculetin on the intestinal inflammatory process and to clarify the mechanism of action of this compound. We also compared its effects with prednisolone and sulphasalazine. Our results demonstrate that treatment with esculetin prevented an increase in malondialdehyde content, counteracted the depletion of glutathione content, reduced epithelial cell apoptosis, reduced the secretion of pro-inflammatory cytokines, such as IL-1β, IL-2 and IFN-γ, in vitro, and reduced the colonic levels of TNF-α and IL-1β in vivo. Additionally, esculetin treatment inhibited MPO and AP activities. These results demonstrated that esculetin produced a more effective intestinal anti-inflammatory effect than sulphasalazine because it was used at a 10-fold lower dose, and it produced effects similar to those created by prednisolone. We suggest that esculetin exerts its activity by inhibiting pro-inflammatory cytokine secretion and increasing the defences against reactive oxygen species. This leads to less migration and/or activation of inflammatory cells, resulting in the improvement of lesions and functions in the intestinal epithelium. This study confirms the intestinal anti-inflammatory activity of esculetin and demonstrates that this compound has both antioxidative and immunomodulatory properties. Therefore, esculetin may be an interesting new anti-inflammatory drug for the treatment of inflammatory bowel disease. Copyright © by BIOLIFE, s.a.s.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
dc.description.sponsorshipSpanish Ministry of Science and Innovation-
dc.description.sponsorshipEuropean Union-
dc.description.sponsorshipJunta de Andalucia-
dc.description.sponsorshipInstituto de Salud Carlos III-
dc.format.extent433-446-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectApoptosis-
dc.subjectEsculetin-
dc.subjectIBD-
dc.subjectMetalloproteinase-
dc.subjectTNBS-
dc.subjectalkaline phosphatase-
dc.subjectesculetin-
dc.subjectgamma interferon-
dc.subjectglutathione-
dc.subjectinterleukin 1beta-
dc.subjectinterleukin 2-
dc.subjectmalonaldehyde-
dc.subjectmyeloperoxidase-
dc.subjectprednisolone-
dc.subjectreactive oxygen metabolite-
dc.subjectsalazosulfapyridine-
dc.subjecttumor necrosis factor alpha-
dc.subjectanimal model-
dc.subjectantiinflammatory activity-
dc.subjectapoptosis-
dc.subjectcolitis-
dc.subjectcytokine release-
dc.subjectdrug effect-
dc.subjectepithelium cell-
dc.subjectimmunomodulation-
dc.subjectintestine epithelium-
dc.titleMechanism and effect of esculetin in an experimental animal model of inflammatory bowel diseaseen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversity of Granada-
dc.description.affiliationDepartment of Pharmacology Institute of Biosciences Univ. Estadual Paulista (UNESP), Botucatu, 18618-970, SP-
dc.description.affiliationDepartment of Physiology Institute of Biosciences Univ. Estadual Paulista - UNESP, Botucatu, SP-
dc.description.affiliationDepartment of Morphology Institute of Biosciences Univ. Estadual Paulista - UNESP, Botucatu, SP-
dc.description.affiliationDepartment of Pharmacology Centre for Biomedical Research University of Granada, Granada-
dc.description.affiliationUnespDepartment of Pharmacology Institute of Biosciences Univ. Estadual Paulista (UNESP), Botucatu, 18618-970, SP-
dc.description.affiliationUnespDepartment of Physiology Institute of Biosciences Univ. Estadual Paulista - UNESP, Botucatu, SP-
dc.description.affiliationUnespDepartment of Morphology Institute of Biosciences Univ. Estadual Paulista - UNESP, Botucatu, SP-
dc.description.sponsorshipIdFAPESP: 03/09324-1-
dc.description.sponsorshipIdFAPESP: 06/55209-9-
dc.description.sponsorshipIdFAPESP: 07/54516-7-
dc.description.sponsorshipIdFAPESP: 11/50824-4-
dc.description.sponsorshipIdFAPESP: 11/50512-2-
dc.description.sponsorshipIdSpanish Ministry of Science and Innovation: SAF2011- 29648-
dc.description.sponsorshipIdJunta de Andalucia: AGR-6826-
dc.description.sponsorshipIdJunta de Andalucia: CTS 164-
dc.identifier.wosWOS:000323914200013-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofEuropean Journal of Inflammation-
dc.identifier.scopus2-s2.0-84884315100-
dc.identifier.orcid0000-0002-8645-3777pt
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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