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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/70541
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dc.contributor.authorGomes, Alessandra Cristina-
dc.contributor.authorGomes Filho, João Eduardo-
dc.contributor.authorOliveira, Sandra Helena Penha de-
dc.date.accessioned2014-05-27T11:23:38Z-
dc.date.accessioned2016-10-25T18:25:55Z-
dc.date.available2014-05-27T11:23:38Z-
dc.date.available2016-10-25T18:25:55Z-
dc.date.issued2008-09-01-
dc.identifierhttp://dx.doi.org/10.1016/j.tripleo.2008.03.022-
dc.identifier.citationOral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, v. 106, n. 3, p. 450-456, 2008.-
dc.identifier.issn1079-2104-
dc.identifier.urihttp://hdl.handle.net/11449/70541-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/70541-
dc.description.abstractObjective: The objective of this study was to investigate the mediators and the resident peritoneal cells involved in the neutrophil migration (NM) induced by mineral trioxide aggregate (MTA) in mice. Study design: MTA (25 mg/cavity) was injected into normal and pretreated peritoneal cavities (PC) with indomethacin (IND), dexamethasone (DEX), BWA4C, U75302, antimacrophage inflammatory protein-2 (MIP-2), and anti-interleukin-1β (IL-1β) antibodies and the NM was determined. The role of macrophage (MO) and mast cells (MAST) was determined by administration of thioglycollate 3% or 48/80 compound, respectively. The concentration of IL-1β and MIP-2 exudates was measured by ELISA. Results: MTA induced dose- and time-dependent NM into mice PC, with the participation of MO and MAST. NM was inhibited by DEX, BWA4C, and U75302, as well as anti-MIP-2 and anti-IL-1β antibodies. In the exudates, IL-1β and MIP-2 were detected. Conclusions: This study suggests that MTA induces NM via a mechanism dependent on MAST and MO mediated by IL-1β, MIP-2, and LTB4. © 2008 Mosby, Inc. All rights reserved.en
dc.format.extent450-456-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectaluminum derivative-
dc.subjectantiinflammatory agent-
dc.subjectcalcium derivative-
dc.subjectCXCL2 chemokine-
dc.subjectinterleukin 1beta-
dc.subjectleukotriene B4-
dc.subjectmineral trioxide aggregate-
dc.subjectoxide-
dc.subjectroot canal filling material-
dc.subjectsilicate-
dc.subjectanimal-
dc.subjectBagg albino mouse-
dc.subjectcytology-
dc.subjectdrug combination-
dc.subjectdrug effect-
dc.subjectmacrophage-
dc.subjectmast cell-
dc.subjectmouse-
dc.subjectneutrophil chemotaxis-
dc.subjectperitoneal cavity-
dc.subjectphysiology-
dc.subjectAluminum Compounds-
dc.subjectAnimals-
dc.subjectAnti-Inflammatory Agents-
dc.subjectCalcium Compounds-
dc.subjectChemokine CXCL2-
dc.subjectDrug Combinations-
dc.subjectInterleukin-1beta-
dc.subjectLeukotriene B4-
dc.subjectMacrophages-
dc.subjectMast Cells-
dc.subjectMice-
dc.subjectMice, Inbred BALB C-
dc.subjectNeutrophil Infiltration-
dc.subjectOxides-
dc.subjectPeritoneal Cavity-
dc.subjectRoot Canal Filling Materials-
dc.subjectSilicates-
dc.titleMTA-induced neutrophil recruitment: a mechanism dependent on IL-1β, MIP-2, and LTB4en
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Basic Sciences Araçatuba Dentistry School São Paulo State University, Araçatuba, SP-
dc.description.affiliationEndodontics Department Araçatuba Dentistry School São Paulo State University, Araçatuba, SP-
dc.description.affiliationUnespDepartment of Basic Sciences Araçatuba Dentistry School São Paulo State University, Araçatuba, SP-
dc.description.affiliationUnespEndodontics Department Araçatuba Dentistry School São Paulo State University, Araçatuba, SP-
dc.identifier.doi10.1016/j.tripleo.2008.03.022-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofOral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology-
dc.identifier.scopus2-s2.0-49049116490-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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