Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions
•The striatal DA depletion observed in the untreated 6-OHDA group.•The decreased locomotor activity and increased apomorphine-induced behavior.•The decreased immunoreactivity for TH in the striatum of 6-OHDA-lesioned rats.•The increased IL-1beta and TNF-alpha immunoreactivity in the substantia nigra...
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| Veröffentlicht in: | Behavioural brain research 2014-05, Vol.264, p.116-125 |
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| creator | Machado-Filho, João Ananias Correia, Alyne Oliveira Montenegro, Anyssa Brilhante Aires Nobre, Maria Elizabeth Pereira Cerqueira, Gilberto Santos Neves, Kelly Rose Tavares Naffah-Mazzacoratti, Maria da Graça Cavalheiro, Esper Abrão de Castro Brito, Gerly Anne de Barros Viana, Glauce Socorro |
| description | •The striatal DA depletion observed in the untreated 6-OHDA group.•The decreased locomotor activity and increased apomorphine-induced behavior.•The decreased immunoreactivity for TH in the striatum of 6-OHDA-lesioned rats.•The increased IL-1beta and TNF-alpha immunoreactivity in the substantia nigra and striatum of 6-OHDA-lesioned rats.•The increased HDAC immunoreactivity in the striatum and CA1 and CA3 areas of the hippocampus of 6-OHDA-lesioned groups.
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 20mg/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-α, IL-1β 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-α and IL-1β. All these effects points out to a neuroprotective effect of caffeine and its potential benefit in the prevention and treatment of PD. |
| doi_str_mv | 10.1016/j.bbr.2014.01.051 |
| format | Article |
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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 20mg/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-α, IL-1β 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-α and IL-1β. All these effects points out to a neuroprotective effect of caffeine and its potential benefit in the prevention and treatment of PD.</description><identifier>ISSN: 0166-4328</identifier><identifier>EISSN: 1872-7549</identifier><identifier>DOI: 10.1016/j.bbr.2014.01.051</identifier><identifier>PMID: 24525422</identifier><identifier>CODEN: BBREDI</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>3,4-Dihydroxyphenylacetic Acid - metabolism ; 6-OHDA model ; Adrenergic Agents - toxicity ; Adult and adolescent clinical studies ; Animals ; Apomorphine - pharmacology ; Behavior ; Biological and medical sciences ; Brain - metabolism ; Caffeine ; Caffeine - pharmacology ; Caffeine - therapeutic use ; Cytokines - metabolism ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dopamine - metabolism ; Dopamine Agonists - pharmacology ; Dose-Response Relationship, Drug ; Exploratory Behavior - drug effects ; Histone Deacetylases - metabolism ; Male ; Medical sciences ; Motor Activity - drug effects ; Neurology ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Organic mental disorders. Neuropsychology ; Oxidopamine - toxicity ; Parkinson Disease - drug therapy ; Parkinson Disease - etiology ; Parkinson Disease - metabolism ; Parkinson Disease - pathology ; Parkinson's disease ; Pro-inflammatory cytokine ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Rats ; Rats, Wistar ; Tyrosine 3-Monooxygenase - metabolism</subject><ispartof>Behavioural brain research, 2014-05, Vol.264, p.116-125</ispartof><rights>2014 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-477bfca75dfb99cef64c97bd6c0fb968f4ce79bd8b7dc6e11a35ef5a929e4a3f3</citedby><cites>FETCH-LOGICAL-c482t-477bfca75dfb99cef64c97bd6c0fb968f4ce79bd8b7dc6e11a35ef5a929e4a3f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0166432814000655$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28305931$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24525422$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Machado-Filho, João Ananias</creatorcontrib><creatorcontrib>Correia, Alyne Oliveira</creatorcontrib><creatorcontrib>Montenegro, Anyssa Brilhante Aires</creatorcontrib><creatorcontrib>Nobre, Maria Elizabeth Pereira</creatorcontrib><creatorcontrib>Cerqueira, Gilberto Santos</creatorcontrib><creatorcontrib>Neves, Kelly Rose Tavares</creatorcontrib><creatorcontrib>Naffah-Mazzacoratti, Maria da Graça</creatorcontrib><creatorcontrib>Cavalheiro, Esper Abrão</creatorcontrib><creatorcontrib>de Castro Brito, Gerly Anne</creatorcontrib><creatorcontrib>de Barros Viana, Glauce Socorro</creatorcontrib><title>Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions</title><title>Behavioural brain research</title><addtitle>Behav Brain Res</addtitle><description>•The striatal DA depletion observed in the untreated 6-OHDA group.•The decreased locomotor activity and increased apomorphine-induced behavior.•The decreased immunoreactivity for TH in the striatum of 6-OHDA-lesioned rats.•The increased IL-1beta and TNF-alpha immunoreactivity in the substantia nigra and striatum of 6-OHDA-lesioned rats.•The increased HDAC immunoreactivity in the striatum and CA1 and CA3 areas of the hippocampus of 6-OHDA-lesioned groups.
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 20mg/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-α, IL-1β 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-α and IL-1β. All these effects points out to a neuroprotective effect of caffeine and its potential benefit in the prevention and treatment of PD.</description><subject>3,4-Dihydroxyphenylacetic Acid - metabolism</subject><subject>6-OHDA model</subject><subject>Adrenergic Agents - toxicity</subject><subject>Adult and adolescent clinical studies</subject><subject>Animals</subject><subject>Apomorphine - pharmacology</subject><subject>Behavior</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Caffeine</subject><subject>Caffeine - pharmacology</subject><subject>Caffeine - therapeutic use</subject><subject>Cytokines - metabolism</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dopamine - metabolism</subject><subject>Dopamine Agonists - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Exploratory Behavior - drug effects</subject><subject>Histone Deacetylases - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Activity - drug effects</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>Oxidopamine - toxicity</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - etiology</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson's disease</subject><subject>Pro-inflammatory cytokine</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><issn>0166-4328</issn><issn>1872-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2O1DAQhC0EYoeFB-CCfEHaAxlsx7ETcVoNP4u00l7gbDlOm_WQOIvtjJTX4Unp0Qxwg5Ol8lfVrS5CXnK25Yyrt_tt36etYFxuGd-yhj8iG95qUelGdo_JBhlVyVq0F-RZznvGmEToKbkQshGNFGJDfu6s9xAi0AhLmh_SXMCVcAAKqLuS6Rypqu5u3l9XI-QwRxhosqjbBHSCIdiCSr_SDAdIdqTeujKn_IaG6MZlCPEbxdQqRD_aabL4t1K3lvk7DsWUOND7kAvm0gGsg7KONgOa70MfCs7Lz8kTb8cML87vJfn68cOX3U11e_fp8-76tnKyFaWSWvfeWd0Mvu86B15J1-l-UI6hoFovHeiuH9peD04B57ZuwDe2Ex1IW_v6klydcnHdHwvkYqaQHYyjjTAv2XClVd0ILvT_0Ya1SretqhHlJ9SlOecE3jykMNm0Gs7MsUWzN9iiObZoGDdYEHpeneOXHk_8x_G7NgRenwGbnR19stGF_Jdra9Z09THo3YkDvNshQDLZBYgOa0tYrhnm8I81fgHaPr6Z</recordid><startdate>20140501</startdate><enddate>20140501</enddate><creator>Machado-Filho, João Ananias</creator><creator>Correia, Alyne Oliveira</creator><creator>Montenegro, Anyssa Brilhante Aires</creator><creator>Nobre, Maria Elizabeth Pereira</creator><creator>Cerqueira, Gilberto Santos</creator><creator>Neves, Kelly Rose Tavares</creator><creator>Naffah-Mazzacoratti, Maria da Graça</creator><creator>Cavalheiro, Esper Abrão</creator><creator>de Castro Brito, Gerly Anne</creator><creator>de Barros Viana, Glauce Socorro</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QG</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope></search><sort><creationdate>20140501</creationdate><title>Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions</title><author>Machado-Filho, João Ananias ; Correia, Alyne Oliveira ; Montenegro, Anyssa Brilhante Aires ; Nobre, Maria Elizabeth Pereira ; Cerqueira, Gilberto Santos ; Neves, Kelly Rose Tavares ; Naffah-Mazzacoratti, Maria da Graça ; Cavalheiro, Esper Abrão ; de Castro Brito, Gerly Anne ; de Barros Viana, Glauce Socorro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-477bfca75dfb99cef64c97bd6c0fb968f4ce79bd8b7dc6e11a35ef5a929e4a3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3,4-Dihydroxyphenylacetic Acid - metabolism</topic><topic>6-OHDA model</topic><topic>Adrenergic Agents - toxicity</topic><topic>Adult and adolescent clinical studies</topic><topic>Animals</topic><topic>Apomorphine - pharmacology</topic><topic>Behavior</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Caffeine</topic><topic>Caffeine - pharmacology</topic><topic>Caffeine - therapeutic use</topic><topic>Cytokines - metabolism</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dopamine - metabolism</topic><topic>Dopamine Agonists - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Exploratory Behavior - drug effects</topic><topic>Histone Deacetylases - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Motor Activity - drug effects</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Organic mental disorders. Neuropsychology</topic><topic>Oxidopamine - toxicity</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - etiology</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson's disease</topic><topic>Pro-inflammatory cytokine</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Machado-Filho, João Ananias</creatorcontrib><creatorcontrib>Correia, Alyne Oliveira</creatorcontrib><creatorcontrib>Montenegro, Anyssa Brilhante Aires</creatorcontrib><creatorcontrib>Nobre, Maria Elizabeth Pereira</creatorcontrib><creatorcontrib>Cerqueira, Gilberto Santos</creatorcontrib><creatorcontrib>Neves, Kelly Rose Tavares</creatorcontrib><creatorcontrib>Naffah-Mazzacoratti, Maria da Graça</creatorcontrib><creatorcontrib>Cavalheiro, Esper Abrão</creatorcontrib><creatorcontrib>de Castro Brito, Gerly Anne</creatorcontrib><creatorcontrib>de Barros Viana, Glauce Socorro</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Animal Behavior Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Behavioural brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Machado-Filho, João Ananias</au><au>Correia, Alyne Oliveira</au><au>Montenegro, Anyssa Brilhante Aires</au><au>Nobre, Maria Elizabeth Pereira</au><au>Cerqueira, Gilberto Santos</au><au>Neves, Kelly Rose Tavares</au><au>Naffah-Mazzacoratti, Maria da Graça</au><au>Cavalheiro, Esper Abrão</au><au>de Castro Brito, Gerly Anne</au><au>de Barros Viana, Glauce Socorro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Caffeine neuroprotective effects on 6-OHDA-lesioned rats are mediated by several factors, including pro-inflammatory cytokines and histone deacetylase inhibitions</atitle><jtitle>Behavioural brain research</jtitle><addtitle>Behav Brain Res</addtitle><date>2014-05-01</date><risdate>2014</risdate><volume>264</volume><spage>116</spage><epage>125</epage><pages>116-125</pages><issn>0166-4328</issn><eissn>1872-7549</eissn><coden>BBREDI</coden><abstract>•The striatal DA depletion observed in the untreated 6-OHDA group.•The decreased locomotor activity and increased apomorphine-induced behavior.•The decreased immunoreactivity for TH in the striatum of 6-OHDA-lesioned rats.•The increased IL-1beta and TNF-alpha immunoreactivity in the substantia nigra and striatum of 6-OHDA-lesioned rats.•The increased HDAC immunoreactivity in the striatum and CA1 and CA3 areas of the hippocampus of 6-OHDA-lesioned groups.
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 20mg/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-α, IL-1β 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-α and IL-1β. All these effects points out to a neuroprotective effect of caffeine and its potential benefit in the prevention and treatment of PD.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>24525422</pmid><doi>10.1016/j.bbr.2014.01.051</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Behavioural brain research, 2014-05, Vol.264, p.116-125 |
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| subjects | 3,4-Dihydroxyphenylacetic Acid - metabolism 6-OHDA model Adrenergic Agents - toxicity Adult and adolescent clinical studies Animals Apomorphine - pharmacology Behavior Biological and medical sciences Brain - metabolism Caffeine Caffeine - pharmacology Caffeine - therapeutic use Cytokines - metabolism Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dopamine - metabolism Dopamine Agonists - pharmacology Dose-Response Relationship, Drug Exploratory Behavior - drug effects Histone Deacetylases - metabolism Male Medical sciences Motor Activity - drug effects Neurology Neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Organic mental disorders. Neuropsychology Oxidopamine - toxicity Parkinson Disease - drug therapy Parkinson Disease - etiology Parkinson Disease - metabolism Parkinson Disease - pathology Parkinson's disease Pro-inflammatory cytokine Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Rats Rats, Wistar Tyrosine 3-Monooxygenase - metabolism |
| title | 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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