Anti-nociceptive effect of kinin B-1 and B-2 receptor antagonists on peripheral neuropathy induced by paclitaxel in mice

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dc.contributor.author Costa, Robson
dc.contributor.author Motta, Emerson M.
dc.contributor.author Dutra, Rafael C.
dc.contributor.author Manjavachi, Marianne N.
dc.contributor.author Bento, Allisson F.
dc.contributor.author Malinsky, Fernanda R. [UNIFESP]
dc.contributor.author Pesquero, João Bosco [UNIFESP]
dc.contributor.author Calixto, Joao B.
dc.date.accessioned 2016-01-24T14:17:07Z
dc.date.available 2016-01-24T14:17:07Z
dc.date.issued 2011-09-01
dc.identifier http://dx.doi.org/10.1111/j.1476-5381.2011.01408.x
dc.identifier.citation British Journal of Pharmacology. Hoboken: Wiley-Blackwell, v. 164, n. 2B, p. 681-693, 2011.
dc.identifier.issn 0007-1188
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/33981
dc.description.abstract BACKGROUND and PURPOSEIn the current study, we investigated the role of both kinin B-1 and B-2 receptors in peripheral neuropathy induced by the chronic treatment of mice with paclitaxel a widely used chemotherapeutic agent.EXPERIMENTAL APPROACHChemotherapy-evoked hyperalgesia was induced by i.p. injections of paclitaxel (2 mg.kg(-1)) over 5 consecutive days. Mechanical and thermal hyperalgesia were evaluated between 7 and 21 days after the first paclitaxel treatment.KEY RESULTSTreatment with paclitaxel increased both mechanical and thermal hyperalgesia in mice (C57BL/6 and CD1 strains). Kinin receptor deficient mice (B-1, or B-2 receptor knock-out and B1B2 receptor, double knock-out) presented a significant reduction in paclitaxel-induced hypernociceptive responses in comparison to wild-type animals. Treatment of CD1 mice with kinin receptor antagonists (DALBK for B-1 or Hoe 140 for B-2 receptors) significantly inhibited both mechanical and thermal hyperalgesia when tested at 7 and 14 days after the first paclitaxel injection. DALBK and Hoe 140 were also effective against paclitaxel-induced peripheral neuropathy when given intrathecally or i.c.v.. A marked increase in B-1 receptor mRNA was observed in the mouse thalamus, parietal and pre-frontal cortex from 7 days after the first paclitaxel treatment.CONCLUSIONS and IMPLICATIONSKinins acting on both B-1 and B-2 receptors, expressed in spinal and supra-spinal sites, played a crucial role in controlling the hypernociceptive state caused by chronic treatment with paclitaxel. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Programa de Apoio aos Nucleos de Excelencia (PRONEX)
dc.description.sponsorship Fundacao de Apoio a Pesquisa do Estado de Santa Catarina (FAPESC)
dc.format.extent 681-693
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof British Journal of Pharmacology
dc.rights Acesso aberto
dc.subject neuropathic pain en
dc.subject chemotherapy en
dc.subject paclitaxel en
dc.subject kinin en
dc.subject B-1 receptor en
dc.subject B-2 receptor en
dc.title Anti-nociceptive effect of kinin B-1 and B-2 receptor antagonists on peripheral neuropathy induced by paclitaxel in mice en
dc.type Artigo
dc.rights.license http://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institution Universidade Federal de Santa Catarina (UFSC)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Fed Santa Catarina, Dept Pharmacol, Ctr Biol Sci, BR-88049900 Florianopolis, SC, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.identifier.doi 10.1111/j.1476-5381.2011.01408.x
dc.description.source Web of Science
dc.identifier.wos WOS:000294367700024



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