Modulation of inflammatory response by selective inhibition of cyclooxygenase-1 and cyclooxygenase-2 in acute kidney injury

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dc.contributor.authorFeitoza, Carla Q. [UNIFESP]
dc.contributor.authorSemedo, Patricia [UNIFESP]
dc.contributor.authorGoncalves, Giselle M. [UNIFESP]
dc.contributor.authorCenedeze, Marcos A. [UNIFESP]
dc.contributor.authorPinheiro, Helady S.
dc.contributor.authorPavao dos Santos, Oscar Fernando [UNIFESP]
dc.contributor.authorLandgraf, Richardt Gama [UNIFESP]
dc.contributor.authorPacheco-Silva, Alvaro [UNIFESP]
dc.contributor.authorSaraiva Camara, Niels Olsen [UNIFESP]
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Fed Juiz de Fora
dc.contributor.institutionHosp Israelita Albert Einstein
dc.date.accessioned2016-01-24T13:59:23Z
dc.date.available2016-01-24T13:59:23Z
dc.date.issued2010-03-01
dc.description.abstractThis work explored the role of inhibition of cyclooxygenases (COXs) in modulating the inflammatory response triggered by acute kidney injury.C57Bl/6 mice were used.Animals were treated or not with indomethacin (IMT) prior to injury (days -1 and 0).Animals were subjected to 45 min of renal pedicle occlusion and sacrificed at 24 h after reperfusion. Serum creatinine and blood urea nitrogen, reactive oxygen species (ROS), kidney myeloperoxidase (MPO) activity, and prostaglandin E2 (PGE(2)) levels were analyzed. Tumor necrosis factor (TNF)-alpha, t-bet, interleukin (IL)-10, IL-1 beta, heme oxygenase (HO)-1, and prostaglandin E synthase (PGES) messenger RNA (mRNA) were studied. Cytokines were quantified in serum.IMT-treated animals presented better renal function with less acute tubular necrosis and reduced ROS and MPO production. Moreover, the treatment was associated with lower expression of TNF-alpha, PGE(2), PGES, and t-bet and upregulation of HO-1 and IL-10. This profile was mirrored in serum, where inhibition of COXs significantly decreased interferon (IFN)-gamma, TNF-alpha, and IL-12 p70 and upregulated IL-10.COXs seem to play an important role in renal ischemia and reperfusion injury, involving the secretion of pro-inflammatory cytokines, activation of neutrophils, and ROS production. Inhibition of COX pathway is intrinsically involved with cytoprotection.en
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Immunol, Transplantat Immunobiol Lab, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Div Nephrol, Expt & Clin Immunol Lab, São Paulo, Brazil
dc.description.affiliationUniv Fed Juiz de Fora, Div Nephrol, Juiz de Fora, MG, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biol Sci, São Paulo, Brazil
dc.description.affiliationHosp Israelita Albert Einstein, Inst Ensino & Pesquisa, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Nephrol, Expt & Clin Immunol Lab, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biol Sci, São Paulo, Brazil
dc.description.sourceWeb of Science
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.sponsorshipIDFAPESP: 04/08311-4
dc.description.sponsorshipIDFAPESP: 07/07139-3 e 06/03982-5
dc.format.extent167-175
dc.identifierhttp://dx.doi.org/10.1007/s00011-009-0083-x
dc.identifier.citationInflammation Research. Basel: Birkhauser Verlag Ag, v. 59, n. 3, p. 167-175, 2010.
dc.identifier.doi10.1007/s00011-009-0083-x
dc.identifier.issn1023-3830
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/32316
dc.identifier.wosWOS:000274331800001
dc.language.isoeng
dc.publisherBirkhauser Verlag Ag
dc.relation.ispartofInflammation Research
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectCyclooxygenaseen
dc.subjectRenal ischemia and reperfusion injuryen
dc.subjectCytokinesen
dc.subjectHeme oxygenase 1en
dc.titleModulation of inflammatory response by selective inhibition of cyclooxygenase-1 and cyclooxygenase-2 in acute kidney injuryen
dc.typeinfo:eu-repo/semantics/article
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