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dc.contributor.authorGentile, Luciana Boffoni [UNESP]
dc.contributor.authorQueiroz-Hazarbassanov, Nicolle
dc.contributor.authorMassoco, Cristina de Oliveira
dc.contributor.authorFecchio, Denise [UNESP]
dc.date.accessioned2015-12-07T15:31:43Z
dc.date.available2015-12-07T15:31:43Z
dc.date.issued2015
dc.identifierhttp://dx.doi.org/10.1155/2015/924028
dc.identifier.citationMediators Of Inflammation, v. 2015, p. 1-8, 2015.
dc.identifier.issn1466-1861
dc.identifier.urihttp://hdl.handle.net/11449/131115
dc.description.abstractThe aim of the present study was to investigate the influence of a nonselective COX1/COX2 inhibitor (indomethacin) on tumor growth of Ehrlich Ascites Tumor (EAT) in mice, using as parameters the tumor growth and cytokine profile. Mice were inoculated with EAT cells and treated with indomethacin. After 1, 3, 6, 10, and 13 days the animals were evaluated for the secretion of TNFα, IL-1α, IL-2, IL-4, IL-6, IL-10, and IL-13 and PGE2 level in peritoneal cavity. The results have shown that EAT induces PGE2 production and increases tumor cells number from the 10th day. The cytokine profile showed EAT induces production of IL-6 from 10th day and of IL-2 on 13th day; the other studied cytokines were not affected in a significant way. The indomethacin treatment of EAT-bearing mice inhibited the tumor growth and PGE2 synthesis from the 10th day. In addition, the treatment of EAT-bearing mice with indomethacin has stimulated the IL-13 production and has significantly inhibited IL-6 in the 13th day of tumor growth. Taken together, the results have demonstrated that EAT growth is modulated by PGE2 and the inhibition of the tumor growth could be partly related to suppression of IL-6 and induction of IL-13.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent1-8
dc.language.isoeng
dc.publisherHindawi Publishing Corporation
dc.relation.ispartofMediators Of Inflammation
dc.sourcePubMed
dc.titleModulation of cytokines production by indomethacin acute dose during the evolution of ehrlich ascites tumor in miceen
dc.typeArtigo
dcterms.rightsHolderHindawi Publishing Corporation
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal do Rio de Janeiro (UFRJ)
dc.description.affiliationLaboratory of Glycobiology, Carlos Chagas Filho Biophysics Institute (IBCCF), Federal University of Rio de Janeiro (UFRJ), 21941-902 Rio de Janeiro, RJ, Brazil
dc.description.affiliationApplied Pharmacology and Toxicology Laboratory, School of Veterinary Medicine, University of São Paulo, 05508-900 São Paulo, SP, Brazil.
dc.description.affiliationUnespDepartment of Pathology, School of Medicine, São Paulo State University (UNESP), 18618-970 Botucatu, SP, Brazil
dc.identifier.doi10.1155/2015/924028
dc.rights.accessRightsAcesso aberto
dc.description.sponsorshipIdFAPESP: 1998/16096-5
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.filePMC4549603.pdf
dc.identifier.pubmed26347589
dc.identifier.pmcPMC4549603
dc.relation.ispartofsjr1,370
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