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

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

Author Machado-Filho, Joao Ananias Google Scholar
Correia, Alyne Oliveira Google Scholar
Aires Montenegro, Anyssa Brilhante Google Scholar
Pereira Nobre, Maria Elizabeth Google Scholar
Cerqueira, Gilberto Santos Google Scholar
Tavares Neves, Kelly Rose Google Scholar
Naffah-Mazzacoratti, Maria da Graca Autor UNIFESP Google Scholar
Cavalheiro, Esper Abrao Autor UNIFESP Google Scholar
Castro Brito, Gerly Anne de Google Scholar
Barros Viana, Glauce Socorro de Google Scholar
Institution Fac Med Estacio Juazeiro do Norte
Univ Fed Ceara
Universidade Federal de São Paulo (UNIFESP)
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.
Keywords Caffeine
Neuroprotection
Parkinson's disease
Pro-inflammatory cytokine
6-OHDA model
Behavior
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Date 2014-05-01
Published in Behavioural Brain Research. Amsterdam: Elsevier B.V., v. 264, p. 116-125, 2014.
ISSN 0166-4328 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 116-125
Origin http://dx.doi.org/10.1016/j.bbr.2014.01.051
Access rights Closed access
Type Article
Web of Science ID WOS:000333853300013
URI http://repositorio.unifesp.br/handle/11600/37726

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