Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions

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dc.contributor.author Machado-Filho, Joao Ananias
dc.contributor.author Correia, Alyne Oliveira
dc.contributor.author Aires Montenegro, Anyssa Brilhante
dc.contributor.author Pereira Nobre, Maria Elizabeth
dc.contributor.author Cerqueira, Gilberto Santos
dc.contributor.author Tavares Neves, Kelly Rose
dc.contributor.author Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
dc.contributor.author Cavalheiro, Esper Abrao [UNIFESP]
dc.contributor.author Castro Brito, Gerly Anne de
dc.contributor.author Barros Viana, Glauce Socorro de
dc.date.accessioned 2016-01-24T14:37:14Z
dc.date.available 2016-01-24T14:37:14Z
dc.date.issued 2014-05-01
dc.identifier http://dx.doi.org/10.1016/j.bbr.2014.01.051
dc.identifier.citation Behavioural Brain Research. Amsterdam: Elsevier B.V., v. 264, p. 116-125, 2014.
dc.identifier.issn 0166-4328
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/37726
dc.description.abstract Several lines of evidences have shown the inversion association between coffee consumption and Parkinson's disease (PD) development. Caffeine is a methylxanthine known as a non-selective inhibitor of A2A and A1 adenosine receptors in the brain and shown to be a neuroprotective drug. the objectives were to study caffeine effects in a unilateral 6-OHDA model of PD in rats. Male rats were divided into the following groups: sham-operated (SO), striatal 6-OHDA-lesioned and 6-OHDA-lesioned and treated for 2 weeks with caffeine (10 and 20 mg/kg, p.o.). Then, animals were subjected to behavioral (open field and apomorphine-induced rotations), neurochemical (striatal determinations of DA and DOPAC), histological (cresyl violet staining) and immunohistochemical (TH, TNF-alpha, IL-1 beta and HDAC) evaluations. the results showed that while the 6-OHDA group presented a decreased locomotor activity and a high number of apomorphine-induced rotations, these behaviors were partially blocked by caffeine. Caffeine itself increased DA contents and reversed the decrease in striatal DA observed in the 6-OHDA-lesioned group. Furthermore, it improved the hippocampal neuronal viability and significantly increased TH immunoreactivity in the striatum of the 6-OHDA-lesioned group. in addition, caffeine treatment also decreased the number of immunopositive cells for HDAC and pro-inflammatory cytokines TNF-alpha and IL-1 beta. All these effects points out to a neuroprotective effect of caffeine and its potential benefit in the prevention and treatment of PD. (C) 2014 Elsevier B.V. All rights reserved. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 116-125
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Behavioural Brain Research
dc.rights Acesso restrito
dc.subject Caffeine en
dc.subject Neuroprotection en
dc.subject Parkinson's disease en
dc.subject Pro-inflammatory cytokine en
dc.subject 6-OHDA model en
dc.subject Behavior en
dc.title Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Fac Med Estacio Juazeiro do Norte
dc.contributor.institution Univ Fed Ceara
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Fac Med Estacio Juazeiro do Norte, Juazeiro Do Norte, CE, Brazil
dc.description.affiliation Univ Fed Ceara, Fac Med, Fortaleza, Ceara, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Expt Neurol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Expt Neurol, São Paulo, Brazil
dc.identifier.doi 10.1016/j.bbr.2014.01.051
dc.description.source Web of Science
dc.identifier.wos WOS:000333853300013



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