The nitroxyl donor Angeli's salt ameliorates Staphylococcus aureus-induced septic arthritis in mice
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Staurengo-Ferrari, LarissaRuiz-Miyazawa, Kenji W
Pinho-Ribeiro, Felipe A
Domiciano, Talita P
Fattori, Victor
Mizokami, Sandra S
Pelayo, Jacinta S
Bordignon, Juliano
Figueiredo, Florêncio
Casagrande, Rubia
Miranda, Katrina M
Verri, Waldiceu A
Affiliation
Univ Arizona, Dept Chem & BiochemIssue Date
2017-01-01
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ELSEVIER SCIENCE INCCitation
Staurengo-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.Rights
© 2017 Elsevier Inc. All rights reserved.Collection Information
This 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.Abstract
Septic 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.Note
12 month embargo; available online 15 April 2017ISSN
1873-4596PubMed ID
28419865Version
Final accepted manuscriptSponsors
CNPq (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; CAPESae974a485f413a2113503eed53cd6c53
10.1016/j.freeradbiomed.2017.04.016
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