Heme oxygenase 1 and renal ischemia and reperfusion injury: the impact of immunosuppressive drug

Página do item simplificado
dc.contributor.authorGoncalves, Giselle Martins
dc.contributor.authorCenedeze, Marcos Antonio
dc.contributor.authorFeitoza, Carla Quarim
dc.contributor.authorPaula, Carolina Batista de
dc.contributor.authorMacusso, Georgia Daniela
dc.contributor.authorPinheiro, Helady Sanders
dc.contributor.authorAntunes Teixeira, Vicente de Paula
dc.contributor.authorReis, Marlene Antonia dos
dc.contributor.authorPacheco-Silva, Alvaro
dc.contributor.authorCamara, Niels Olsen Saraiva
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniv Fed Uberaba
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:41:40Z
dc.date.available2016-01-24T12:41:40Z
dc.date.issued2006-12-20
dc.description.abstractBackground: Ischemia and reperfusion injury (IRI) is the main etiology of acute renal failure in native and transplanted kidneys. in the transplantation field, immunosuppressive drugs may play an additional role in acute graft dysfunction. Acute cyclosporine nephrotoxicity (ATN) can result from vasoconstriction of the afferent arterioles, which may exacerbate deceased renal transplantation. HO-1 is a protective gene with anti-inflammatory and anti-apoptotic actions. We investigated whether HO-1 played a role in cyclosporine-induced renal dysfunction in an established model of IRLMethods: Cyclosporine (100 mg/kg) was administered to mice before being subjected to 45 min of ischemia. Blood and kidney samples were collected at 24, 48 and 120 h after surgery. Acute tubular necrosis and tubular regeneration were quantified. HO-1 gene transcripts were amplified by real-time PCR.Results: Animals subjected to IRI presented with impaired renal function that peaked at 24 h (2.05 +/- 0.23 mg/dL), decreasing thereafter. Treatment with cyclosporine caused even more renal dysfunction at 48 h, sustained up to 120 h after reperfusion (1.53 +/- 0.6 mg/dL), when compared to the controls (0.63 +/- 0.09 mg/dL, p < 0,05). Cyclosporine delayed tubular regeneration that was normally higher in controls at day 5 (67.0% vs. 37.6%, p < 0.05). HO-1 was markedly up-regulated after IRI, and its expression was decreased by cyclosporine (2.06 folds). However, prior induction of HO-1 by cobalt protoporphyrin improved renal dysfunction.Conclusions: These results demonstrated that cyclosporine used in ischemic injured organs might also negatively affect post-transplantation recovery. (c) 2006 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniv São Paulo, Dept Immunol, Inst Biomed Sci 4, Lab Transplantat Immunol, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniv Fed Uberaba, Dept Pathol, Uberaba, MG, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Lab Imunol Clin & Expt, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Lab Imunol Clin & Expt, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1966-1972
dc.identifierhttp://dx.doi.org/10.1016/j.intimp.2006.07.009
dc.identifier.citationInternational Immunopharmacology. Amsterdam: Elsevier B.V., v. 6, n. 13-14, p. 1966-1972, 2006.
dc.identifier.doi10.1016/j.intimp.2006.07.009
dc.identifier.issn1567-5769
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29316
dc.identifier.wosWOS:000243216400015
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofInternational Immunopharmacology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectischemia and reperfusion injuryen
dc.subjectcyclosporineen
dc.subjectheme oxygenase 1en
dc.titleHeme oxygenase 1 and renal ischemia and reperfusion injury: the impact of immunosuppressive drugen
dc.typeinfo:eu-repo/semantics/article
Arquivos
Coleções
EPM - Artigos