dc.creatorRodrigues, WF
dc.creatorMadeira, MFM
dc.creatorda Silva, TA
dc.creatorClemente-Napimoga, JT
dc.creatorMiguel, CB
dc.creatorDias-da-Silva, VJ
dc.creatorBarbosa-Neto, O
dc.creatorLopes, AH
dc.creatorNapimoga, MH
dc.date2012
dc.dateAPR
dc.date2014-07-30T13:39:00Z
dc.date2015-11-26T16:34:35Z
dc.date2014-07-30T13:39:00Z
dc.date2015-11-26T16:34:35Z
dc.date.accessioned2018-03-28T23:16:50Z
dc.date.available2018-03-28T23:16:50Z
dc.identifierBritish Journal Of Pharmacology. Wiley-blackwell, v. 165, n. 7, n. 2140, n. 2151, 2012.
dc.identifier0007-1188
dc.identifierWOS:000301281700014
dc.identifier10.1111/j.1476-5381.2011.01686.x
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/52715
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/52715
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1271240
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionBACKGROUND AND PURPOSE Bones are widely innervated, suggesting an important role for the sympathetic regulation of bone metabolism, although there are controversial studies. We investigated the effects of propranolol in a model of experimental periodontal disease. EXPERIMENTAL APPROACH Rats were assigned as follows: animals without ligature; ligated animals receiving vehicle and ligated animals receiving 0.1, 5 or 20 mg.kg-1 propranolol. After 30 days, haemodynamic parameters were measured by cardiac catheterization. Gingival tissues were removed and assessed for IL-1 beta, TNF-alpha and cross-linked carboxyterminal telopeptides of type I collagen (CTX) by ELISA, or intercellular adhesion molecule 1 (ICAM-1), receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin (OPG) by Western blot analysis. Sections from the mandibles were evaluated for bone resorption. Also, we analysed the ability of propranolol to inhibit osteoclastogenesis in vitro. RESULTS Propranolol at 0.1 and 5 mg.kg-1 reduced the bone resorption as well as ICAM-1 and RANKL expression. However, only 0.1 mg.kg-1 reduced IL-1 beta, TNF-alpha and CTX levels as well as increased the expression of OPG, but did not alter any of the haemodynamic parameters. Propranolol also suppressed in vitro osteoclast differentiation and resorptive activity by inhibiting the nuclear factor of activated T cells (NFATc) 1 pathway and the expression of tartrate-resistant acid phosphatase (TRAP), cathepsin K and MMP-9. CONCLUSIONS AND IMPLICATIONS Low doses of propranolol suppress bone resorption by inhibiting RANKL-mediated osteoclastogenesis as well as inflammatory markers without affecting haemodynamic parameters.
dc.description165
dc.description7
dc.description2140
dc.description2151
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionPAPE-UNIUBE [2009/001]
dc.descriptionFundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionCNPq [471305/2009-0, 303080/2010-8]
dc.descriptionPAPE-UNIUBE [2009/001]
dc.descriptionFAPEMIG [097/09]
dc.languageen
dc.publisherWiley-blackwell
dc.publisherMalden
dc.publisherEUA
dc.relationBritish Journal Of Pharmacology
dc.relationBr. J. Pharmacol.
dc.rightsfechado
dc.rightshttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.sourceWeb of Science
dc.subjectpropranolol
dc.subjectperiodontal disease
dc.subjectss-blocker
dc.subjectbone
dc.subjectinflammation
dc.subjectSympathetic-nervous-system
dc.subjectOsteogenic-sarcoma Cells
dc.subjectCoronary-heart-disease
dc.subjectPeriodontal-disease
dc.subjectHuman Osteoblasts
dc.subjectBeta-blocker
dc.subjectCathepsin-k
dc.subjectCardiovascular-disease
dc.subjectOral-health
dc.subjectMice
dc.titleLow dose of propranolol down-modulates bone resorption by inhibiting inflammation and osteoclast differentiation
dc.typeArtículos de revistas


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