Mechanisms underlying the nociceptive and inflammatory responses induced by trypsin in the mouse paw

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dc.contributor.authorPaszcuk, Ana Flavia
dc.contributor.authorQuintao, Nara L. M.
dc.contributor.authorFernandes, Elizabeth S.
dc.contributor.authorJuliano, Luiz [UNIFESP]
dc.contributor.authorChapman, Kevin
dc.contributor.authorAndrade-Gordon, Patricia
dc.contributor.authorCampos, Maria Martha
dc.contributor.authorVergnolle, Nathalie
dc.contributor.authorCalixto, Joao B.
dc.contributor.institutionUniversidade Federal de Santa Catarina (UFSC)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionPontificia Univ Catolica Rio Grande do Sul
dc.contributor.institutionUniv Calgary
dc.date.accessioned2016-01-24T13:49:34Z
dc.date.available2016-01-24T13:49:34Z
dc.date.issued2008-02-26
dc.description.abstractIt has been demonstrated that trypsin is able to evoke the classical signals of inflammation, mainly via the activation of proteinase-activated receptor-2 (PAR-2). This study was designed to evaluate the inflammatory and nociceptive responses caused by trypsin injection in the mouse paw. Trypsin produced a dose- and time-related paw edema, a response that was markedly reduced in PAR-2-deficient mice compared to wild-type mice, particularly at the early time-points after trypsin injection. in addition, trypsin produced an increase in myeloperoxidase (MPO) activity, which was significantly reduced in PAR-2-deficient mice. the injection of trypsin into the mouse paw also elicited a dose- and time-dependent spontaneous nociception, as well as thermal and mechanical hypernociceptive responses, which were consistently decreased in mice with genetic deletion of PAR-2. Pharmacological evaluation revealed that edema formation and spontaneous nociception caused by trypsin injection in the mouse paw are mediated by a complex range of mediators. Both edema and nociception seem to rely on the production of neuropeptides, probably involving C-fibre activation and vanilloid receptor-1 (TRPV1), besides the stimulation of kinin B-2 receptors. Edematogenic response is also likely related to the production of cyclooxygenase (COX) metabolites, whereas the mast cell activation appears to be greatly associated to spontaneous nociception. Altogether, the present results indicate that trypsin-induced edema and nociception in the mouse paw represent multi-mediated responses that are largely, but not exclusively, related to the activation of PAR-2. These pieces of evidence provide new insights on the role of trypsin in pain and inflammation. (C) 2007 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniv Fed Santa Catarina, Ctr Biol Sci, Dept Pharmacol, BR-88049900 Florianopolis, SC, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, São Paulo, Brazil
dc.description.affiliationPontificia Univ Catolica Rio Grande do Sul, Sch Dent, Porto Alegre, RS, Brazil
dc.description.affiliationUniv Calgary, Dept Pharmacol & Therapeut, Calgary, AB, Canada
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent204-215
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2007.11.025
dc.identifier.citationEuropean Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 581, n. 1-2, p. 204-215, 2008.
dc.identifier.doi10.1016/j.ejphar.2007.11.025
dc.identifier.issn0014-2999
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30450
dc.identifier.wosWOS:000253575900025
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Pharmacology
dc.rightsAcesso restrito
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjecttrypsinen
dc.subjectinflammationen
dc.subjectedemaen
dc.subjectnociceptionen
dc.subjectPAR-2en
dc.subject(Mouse)en
dc.titleMechanisms underlying the nociceptive and inflammatory responses induced by trypsin in the mouse pawen
dc.typeArtigo
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