Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

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dc.contributor.authorPessoa, Edson de Andrade [UNIFESP]
dc.contributor.authorConvento, Marcia.Bastos [UNIFESP]
dc.contributor.authorSilva, Ronaldo Goncalves da [UNIFESP]
dc.contributor.authorOliveira, Accary Souza Bulle [UNIFESP]
dc.contributor.authorBorges, Fernanda Teixeira [UNIFESP]
dc.contributor.authorSchor, Nestor [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2015-06-14T13:41:01Z
dc.date.available2015-06-14T13:41:01Z
dc.date.issued2009-07-01
dc.description.abstractNephrotoxicity is the main side effect of antibiotics such as gentamicin. Preconditioning has been reported to protect against injuries as ischemia/reperfusion. The objective of the present study was to determine the effect of preconditioning with gentamicin on LLC-PK1 cells. Preconditioning was induced in LLC-PK1 cells by 24-h exposure to 2.0 mM gentamicin (G/IU). After 4 or 15 days of preconditioning, cells were again exposed to gentamicin (2.0 mM) and compared to untreated control or G/IU cells. Necrosis and apoptosis were assessed by acridine orange and HOESCHT 33346. Nitric oxide (NO) and endothelin-1 were assessed by the Griess method and available kit. Heat shock proteins were analyzed by Western blotting. After 15 days of preconditioning, LLC-PK1 cells exhibited a significant decrease in necrosis (23.5 ± 4.3 to 6.5 ± 0.3%) and apoptosis (23.5 ± 4.3 to 6.5 ± 2.1%) and an increase in cell proliferation compared to G/IU. NO (0.177 ± 0.05 to 0.368 ± 0.073 µg/mg protein) and endothelin-1 (1.88 ± 0.47 to 2.75 ± 0.53 pg/mL) production significantly increased after 15 days of preconditioning compared to G/IU. No difference in inducible HSP 70, constitutive HSC 70 or HSP 90 synthesis in tubular cells was observed after preconditioning with gentamicin. The present data suggest that preconditioning with gentamicin has protective effects on proximal tubular cells, that involved NO synthesis but not reduction of endothelin-1 or production of HSP 70, HSC 70, or HSP 90. We conclude that preconditioning could be a useful tool to prevent the nephrotoxicity induced by gentamicin.en
dc.description.affiliationUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de Medicina
dc.description.affiliationUnifespUNIFESP, EPM, Depto. de Medicina
dc.description.sourceSciELO
dc.format.extent614-620
dc.identifierhttp://dx.doi.org/10.1590/S0100-879X2009005000005
dc.identifier.citationBrazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 42, n. 7, p. 614-620, 2009.
dc.identifier.doi10.1590/S0100-879X2009005000005
dc.identifier.fileS0100-879X2009000700005.pdf
dc.identifier.issn0100-879X
dc.identifier.scieloS0100-879X2009000700005
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/5129
dc.identifier.wosWOS:000267703600005
dc.language.isoeng
dc.publisherAssociação Brasileira de Divulgação Científica
dc.relation.ispartofBrazilian Journal of Medical and Biological Research
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPre-conditioningen
dc.subjectGentamicinen
dc.subjectNitric oxideen
dc.subjectLLC-PK1 cellsen
dc.subjectAcute kidney injuryen
dc.subjectApoptosisen
dc.titleGentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock proteinen
dc.typeinfo:eu-repo/semantics/article
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