Cyclooxygenase 1 and/or 2 blockade ameliorates the renal tissue damage triggered by ischemia and reperfusion injury

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dc.contributor.author Feitoza, C. Q.
dc.contributor.author Camara, NOS
dc.contributor.author Pinheiro, H. S.
dc.contributor.author Goncalves, G. M.
dc.contributor.author Cenedeze, M. A.
dc.contributor.author Pacheco-Silva, A.
dc.contributor.author Santos, OFP
dc.date.accessioned 2016-01-24T12:37:33Z
dc.date.available 2016-01-24T12:37:33Z
dc.date.issued 2005-01-01
dc.identifier http://dx.doi.org/10.1016/j.intimp.2004.09.024
dc.identifier.citation International Immunopharmacology. Amsterdam: Elsevier B.V., v. 5, n. 1, p. 79-84, 2005.
dc.identifier.issn 1567-5769
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/28082
dc.description.abstract Ischemia-reperfusion injury (IRI) is a common event in organ transplantation. being implicated as a potential contributor for the development of chronic allograft nephropathy. There are new evidences showing a tissue inflammatory response following renal IRI Cyclooxygenases (COX) 1 and 2 can be detected in tissue submitted to IRI and may have impact on organ function outcome. We evaluated the role of COX inhibition on the renal tissue damage that follows M. Mice were submitted to 45 min of renal pedicle ligature and allowed to reperfuse for 24, 48, 72 and 120 h. Blood and kidney samples were collected at reperfusion times. mRNA was extracted from the kidney samples to amplify, COX-1: COX-2 and beta-actin genes. Animals were pretreated with indomethacin or rofecoxib before the surgery. Indomethacin treatment induced a better renal function (serum urea) when compared to control animals at 24, 48 and 72 h (219 +/- 54.5 vs. 338 +/- 51 mg/dl: 106 +/- 51 vs. 326 +/- 86 mg/dl; 94 +/- 14 vs. 138 +/- 38 mg/dl, respectively). Surprisingly, rofecoxib use was associated with even better renal improvement following IR. Animals treated with the later drug showed lower urea values at 24 h post reperfusion compared to indomethacin-treated animals (128 +/- 33 vs. 219 +/- 54.5 mg/dl, P < 0.05). Blockade of COX-1 and -2 resulted in a decrease of tubular necrosis. mRNA COX-2 was up-regulated post IRI and considerable inhibited after indomethacin or rofecoxib treatment. Our data show COX-1/-2 participates in the inflammatory tissue response to IR injury and its inhibition is associated with an improvement in renal function. (C) 2004 Elsevier B.V. All rights reserved. en
dc.format.extent 79-84
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof International Immunopharmacology
dc.rights Acesso restrito
dc.subject ischemia and reperfusion injury en
dc.subject acute renal failure en
dc.subject cyclooxygenase en
dc.title Cyclooxygenase 1 and/or 2 blockade ameliorates the renal tissue damage triggered by ischemia and reperfusion injury en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Clin & Expt Immunol Lab, Dept Med, Disciplina Nefrol,Hosp Rim & Hipertensao, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Clin & Expt Immunol Lab, Dept Med, Disciplina Nefrol,Hosp Rim & Hipertensao, BR-04023900 São Paulo, Brazil
dc.identifier.doi 10.1016/j.intimp.2004.09.024
dc.description.source Web of Science
dc.identifier.wos WOS:000226615400011



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