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dc.contributor.authorStaurengo-Ferrari, Larissa
dc.contributor.authorRuiz-Miyazawa, Kenji W
dc.contributor.authorPinho-Ribeiro, Felipe A
dc.contributor.authorDomiciano, Talita P
dc.contributor.authorFattori, Victor
dc.contributor.authorMizokami, Sandra S
dc.contributor.authorPelayo, Jacinta S
dc.contributor.authorBordignon, Juliano
dc.contributor.authorFigueiredo, Florêncio
dc.contributor.authorCasagrande, Rubia
dc.contributor.authorMiranda, Katrina M
dc.contributor.authorVerri, Waldiceu A
dc.date.accessioned2019-03-13T17:54:24Z
dc.date.available2019-03-13T17:54:24Z
dc.date.issued2017-01-01
dc.identifier.citationStaurengo-Ferrari, L., Ruiz-Miyazawa, K. W., Pinho-Ribeiro, F. A., Domiciano, T. P., Fattori, V., Mizokami, S. S., ... & Miranda, K. M. (2017). The nitroxyl donor Angeli's salt ameliorates Staphylococcus aureus-induced septic arthritis in mice. Free Radical Biology and Medicine, 108, 487-499.en_US
dc.identifier.issn1873-4596
dc.identifier.pmid28419865
dc.identifier.doi10.1016/j.freeradbiomed.2017.04.016
dc.identifier.urihttp://hdl.handle.net/10150/631839
dc.description.abstractSeptic arthritis is a severe and rapidly debilitating disease associated with severe joint pain, inflammation and oxidative stress. Nitroxyl (HNO) has become a nitrogen oxide of significant interest due to its pharmacological endpoints that are potentially favorable for treating varied diseases. However, whether HNO also serves as a treatment to septic arthritis is currently unknown. The aim of this study was to investigate the effect of the HNO donor, Angeli's salt (AS), in the outcome of chronic Staphylococcus aureus (S. aureus)-induced septic arthritis in mice. Daily treatment with AS inhibited mechanical hyperalgesia and inflammation (edema, leukocyte migration, cytokines release and NF-κB activation, and oxidative stress) resulting in reduced disease severity (clinical course, histopathological changes, proteoglycan levels in the joints, and osteoclastogenesis). In addition, AS decreased the number of S. aureus colony forming unities in synovial tissue, enhanced the bactericidal effect of macrophages and inhibited the worsening of systemic inflammatory response (leukocyte counts in the lung and systemic proinflammatory cytokine concentration). Our results suggest for the first time the therapeutic potential of AS in a model of septic arthritis by mechanisms involving microbicidal effects, anti-inflammatory actions and reduction of disease severity.en_US
dc.description.sponsorshipCNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico); MCTI/SETI/Fundacao Araucaria (Ministerio da Ciencia, Tecnologia e Inovacao/Secretaria da Ciencia, Tecnologia, e Ensino Superior do Parana/Fundacao Araucaria); Decit/SCTIE/MS (Departamento de Ciencia e Tecnologia da Secretaria de Ciencia, Tecnologia e Insumos Estrategicos, Ministerio da Saude); Fundacao Araucaria; Coordenadoria de Aperfeicoamento de Pessoal de Nivel Superior (CAPES); INCT (National Institutes of Science and Technology) - MCTI/CNPq/CAPES/Fundacao Araucaria, Brazil; CAPES [PDSE - 99999.007507/2014-03]; CNPq [161279/2015-5]; CAPES/Fundacao Araucaria; CAPESen_US
dc.language.isoenen_US
dc.publisherELSEVIER SCIENCE INCen_US
dc.rights© 2017 Elsevier Inc. All rights reserved.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectAngeli's salten_US
dc.subjectCytokinesen_US
dc.subjectLeukocytesen_US
dc.subjectNitric oxideen_US
dc.subjectNitroxylen_US
dc.subjectOxidative stressen_US
dc.subjectPainen_US
dc.subjectSeptic arthritisen_US
dc.titleThe nitroxyl donor Angeli's salt ameliorates Staphylococcus aureus-induced septic arthritis in miceen_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Dept Chem & Biochemen_US
dc.identifier.journalFREE RADICAL BIOLOGY AND MEDICINEen_US
dc.description.note12 month embargo; available online 15 April 2017en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal accepted manuscripten_US
dc.source.journaltitleFree radical biology & medicine
refterms.dateFOA2018-04-15T00:00:00Z


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