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[PMID]:29442034
[Au] Autor:Li J; Ma L; Fan Y; Zhang Y; Sun D; Wu B
[Ti] Título:Crosstalk between 6-OHDA-induced autophagy and apoptosis in PC12 cells is mediated by phosphorylation of Raf-1/ERK1/2.
[So] Source:Pharmazie;71(8):465-471, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a degenerative brain disorder characterized by motor symptoms and loss of dopaminergic (DA) neurons in the substantia nigra. The mechanisms for DA cell death in PD have been extensively investigated using PC12 cells treated with a dopamine neurotoxin 6-hydroxydopamine (6-OHDA). 6-OHDA may induce both autophagy and apoptosis in PC12 cells. However, it remains unclear whether crosstalk occurs between autophagy and apoptosis in PC12 cells treated with 6-OHDA and whether Raf-1/ERK1/2 and their phosphorylation status play a role in autophagy. In this study, we used MDC staining assay and flow cytometry and found that 6-OHDA induced autophagy in PC12 cells. This induction was inhibited by the autophagy inhibitor 3-MA. Our electron microscopy observations also supported 6-OHDA induced autophagy in PC12 cells. Apoptosis of PC12 cells was increased with inhibition of autophagy by 3-MA. In addition, Inhibition of Raf-1 resulted in a decreased 6-OHDA-induced autophagy rate among PC12 cells. Phosphorylation levels of Raf-1 and ERK1/2 were increased in PC12 cells treated with 6-OHDA and inhibited by co-treatment with 6-OHDA and 3-MA. These data suggest that crosstalk between 6-OHDA-induced apoptosis and autophagy in PC12 cells may be regulated via the Raf-1/ERK1/2 signaling pathway. Our data suggest a mechanism for 6-OHDA toxicity in PC12 cells, contributing to our understanding of the pathogenesis of PD.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Hidroxidopaminas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/metabolismo
Receptor Cross-Talk/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Animais
Sobrevivência Celular/efeitos dos fármacos
Células PC12
Proteínas Proto-Oncogênicas c-raf/efeitos dos fármacos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxydopamines); 72055-62-0 (3-methyladenosine); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.1 (Raf1 protein, rat); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6586


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[PMID]:28847810
[Au] Autor:Sharott A; Vinciati F; Nakamura KC; Magill PJ
[Ad] Endereço:Medical Research Council Brain Network Dynamics Unit, University of Oxford, Oxford OX1 3TH, United Kingdom, and andrew.sharott@pharm.ox.ac.uk peter.magill@pharm.ox.ac.uk.
[Ti] Título:A Population of Indirect Pathway Striatal Projection Neurons Is Selectively Entrained to Parkinsonian Beta Oscillations.
[So] Source:J Neurosci;37(41):9977-9998, 2017 Oct 11.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classical schemes of basal ganglia organization posit that parkinsonian movement difficulties presenting after striatal dopamine depletion stem from the disproportionate firing rates of spiny projection neurons (SPNs) therein. There remains, however, a pressing need to elucidate striatal SPN firing in the context of the synchronized network oscillations that are abnormally exaggerated in cortical-basal ganglia circuits in parkinsonism. To address this, we recorded unit activities in the dorsal striatum of dopamine-intact and dopamine-depleted rats during two brain states, respectively defined by cortical slow-wave activity (SWA) and activation. Dopamine depletion escalated striatal net output but had contrasting effects on "direct pathway" SPNs (dSPNs) and "indirect pathway" SPNs (iSPNs); their firing rates became imbalanced, and they disparately engaged in network oscillations. Disturbed striatal activity dynamics relating to the slow (∼1 Hz) oscillations prevalent during SWA partly generalized to the exaggerated beta-frequency (15-30 Hz) oscillations arising during cortical activation. In both cases, SPNs exhibited higher incidences of phase-locked firing to ongoing cortical oscillations, and SPN ensembles showed higher levels of rhythmic correlated firing, after dopamine depletion. Importantly, in dopamine-depleted striatum, a widespread population of iSPNs, which often displayed excessive firing rates and aberrant phase-locked firing to cortical beta oscillations, preferentially and excessively synchronized their firing at beta frequencies. Conversely, dSPNs were neither hyperactive nor synchronized to a large extent during cortical activation. These data collectively demonstrate a cell type-selective entrainment of SPN firing to parkinsonian beta oscillations. We conclude that a population of overactive, excessively synchronized iSPNs could orchestrate these pathological rhythms in basal ganglia circuits. Chronic depletion of dopamine from the striatum, a part of the basal ganglia, causes some symptoms of Parkinson's disease. Here, we elucidate how dopamine depletion alters striatal neuron firing , with an emphasis on defining whether and how spiny projection neurons (SPNs) engage in the synchronized beta-frequency (15-30 Hz) oscillations that become pathologically exaggerated throughout basal ganglia circuits in parkinsonism. We discovered that a select population of so-called "indirect pathway" SPNs not only fire at abnormally high rates, but are also particularly prone to being recruited to exaggerated beta oscillations. Our results provide an important link between two complementary theories that explain the presentation of disease symptoms on the basis of changes in firing rate or firing synchronization/rhythmicity.
[Mh] Termos MeSH primário: Ritmo beta
Corpo Estriado/fisiopatologia
Vias Neurais/fisiopatologia
Neurônios/patologia
Transtornos Parkinsonianos/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Gânglios da Base/fisiopatologia
Córtex Cerebral/patologia
Córtex Cerebral/fisiopatologia
Corpo Estriado/patologia
Dopamina/metabolismo
Hidroxidopaminas
Masculino
Vias Neurais/patologia
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxydopamines); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0658-17.2017


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[PMID]:27763504
[Au] Autor:Feng CW; Hung HC; Huang SY; Chen CH; Chen YR; Chen CY; Yang SN; Wang HD; Sung PJ; Sheu JH; Tsui KH; Chen WF; Wen ZH
[Ad] Endereço:Doctoral Degree Program in Marine Biotechnology, National Sun Yat-Sen University, 70 Lien-Hai Road, Kaohsiung 804, Taiwan. qscjuejuejue@gmail.com.
[Ti] Título:Neuroprotective Effect of the Marine-Derived Compound 11-Dehydrosinulariolide through DJ-1-Related Pathway in In Vitro and In Vivo Models of Parkinson's Disease.
[So] Source:Mar Drugs;14(10), 2016 Oct 17.
[Is] ISSN:1660-3397
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.
[Mh] Termos MeSH primário: Antiparkinsonianos/farmacologia
Diterpenos/farmacologia
Fármacos Neuroprotetores/farmacologia
Doença de Parkinson/tratamento farmacológico
Proteína Desglicase DJ-1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Técnicas de Silenciamento de Genes
Seres Humanos
Hidroxidopaminas
Masculino
Mitocôndrias/química
Doença de Parkinson Secundária/induzido quimicamente
Doença de Parkinson Secundária/tratamento farmacológico
Proteína Desglicase DJ-1/biossíntese
Proteína Desglicase DJ-1/genética
RNA Interferente Pequeno/farmacologia
Ratos
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
Natação
Tirosina 3-Mono-Oxigenase/metabolismo
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (11-dehydrosinulariolide); 0 (Antiparkinson Agents); 0 (Diterpenes); 0 (Hydroxydopamines); 0 (Neuroprotective Agents); 0 (RNA, Small Interfering); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:26612350
[Au] Autor:Ma C; Pan Y; Yang Z; Meng Z; Sun R; Wang T; Fei Y; Fan W
[Ad] Endereço:Department of Neurology, First Hospital and Clinical College of Harbin Medical University, Harbin, Heilongjiang Province 150001, China.
[Ti] Título:Pre-administration of BAX-inhibiting peptides decrease the loss of the nigral dopaminergic neurons in rats.
[So] Source:Life Sci;144:113-20, 2016 Jan 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: In this study, we investigated the effects of Bax-inhibiting peptide (Bip)-V5, an anti-apoptosis membrane-permeable peptide, on the 6-hydroxydopamine (6-OHDA) induced Parkinson's disease (PD) model rats. MATERIALS AND METHODS: Rats were randomly divided into five groups: Control, 6-OHDA only, Vehicle+6-OHDA, zVAD+6-OHDA, and V5+6-OHDA, that rats were preadministrated with different reagents before 6-OHDA administration. KEY FINDINGS: The result showed that intrastriatal preadministration of Bip-V5 significantly decreased the amphetamine-induced rotation of the 6-OHDA model rats and the loss of the nigral dopaminergic (DA) neurons. Moreover, Bip-V5 intrastriatal preadministration not only significantly decreased the expression of activated caspase 9 and activated caspase 3 but also decreased the enhanced expression of AIF and its nuclear translocation in the SNpc. The results in our study provide the first experimental evidence that both caspase-dependent and AIF-dependent apoptosis pathways are involved in the loss of the nigral DA neurons caused by intrastriatal administration of 6-OHDA, and intrastriatal preadministration of Bip-V5 can inhibit the above two apoptosis pathways to protect the nigral DA neurons. SIGNIFICANCE: Our results provide a new idea that Bax-inhibiting peptide may be a promising preventive or therapeutic method for PD.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Oligopeptídeos/farmacologia
Substância Negra/citologia
Substância Negra/efeitos dos fármacos
Proteína X Associada a bcl-2/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anfetamina/farmacologia
Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Fator de Indução de Apoptose/biossíntese
Fator de Indução de Apoptose/genética
Comportamento Animal/efeitos dos fármacos
Caspase 3/biossíntese
Caspase 3/genética
Caspase 9/biossíntese
Caspase 9/genética
Inibidores da Captação de Dopamina/farmacologia
Hidroxidopaminas
Masculino
Doença de Parkinson Secundária/induzido quimicamente
Doença de Parkinson Secundária/patologia
Transporte Proteico/efeitos dos fármacos
Ratos
Ratos Wistar
Rotação
Proteína X Associada a bcl-2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apoptosis Inducing Factor); 0 (Bax protein, rat); 0 (Dopamine Uptake Inhibitors); 0 (Hydroxydopamines); 0 (Neuroprotective Agents); 0 (Oligopeptides); 0 (Pdcd8 protein, rat); 0 (Val-Pro-Met-Leu-Lys); 0 (bcl-2-Associated X Protein); CK833KGX7E (Amphetamine); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Casp9 protein, rat); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:160106
[Lr] Data última revisão:
160106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151128
[St] Status:MEDLINE


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[PMID]:26481946
[Au] Autor:Beppe GJ; Dongmo AB; Foyet HS; Dimo T; Mihasan M; Hritcu L
[Ad] Endereço:Laboratory of Animal Physiology, Faculty of Science, University of Yaoundé I, PO Box, 812, Yaoundé, Cameroon. galbajeanbeppe@yahoo.com.
[Ti] Título:The aqueous extract of Albizia adianthifolia leaves attenuates 6-hydroxydopamine-induced anxiety, depression and oxidative stress in rat amygdala.
[So] Source:BMC Complement Altern Med;15:374, 2015 Oct 19.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: While the Albizia adianthifolia (Schumach.) W. Wright (Fabaceae) is a traditional herb largely used in the African traditional medicine as analgesic, purgative, antiinflammatory, antioxidant, antimicrobial, memory-enhancer, anxiolytic and antidepressant drug, there are no scientific data that clarify the anxiolytic and antidepressant-like effects in 6-hydroxydopamine (6-OHDA)-lesioned animal model of Parkinson's disease. This study was undertaken in order to identify the effects of aqueous extract of A. adianthifolia leaves on 6-hydroxydopamine-induced anxiety, depression and oxidative stress in the rat amygdala. METHODS: The effect of the aqueous extract of A. adianthifolia leaves (150 and 300 mg/kg, orally, daily, for 21 days) on anxiety and depression was assessed using elevated plus-maze and forced swimming tests, as animal models of anxiety and depression. Also, the antioxidant activity in the rat amygdala was assessed using assessed using superoxide dismutase, glutathione peroxidase and catalase specific activities, the total content of the reduced glutathione, protein carbonyl and malondialdehyde levels. Statistical analyses were performed using by one-way analysis of variance (ANOVA). Significant differences were determined by Tukey's post hoc test. F values for which p < 0.05 were regarded as statistically significant. Pearson's correlation coefficient and regression analysis were used in order to evaluate the connection between behavioral measures, the antioxidant defence and lipid peroxidation. RESULTS: 6-OHDA-lesioned rats exhibited the following: decrease of the exploratory activity, the percentage of the time spent and the number of entries in the open arm within elevated plus-maze test and decrease of swimming time and increase of immobility time within forced swimming test. Administration of the aqueous extract significantly exhibited anxiolytic- and antidepressant-like effects and also antioxidant potential in the rat amygdala. CONCLUSIONS: Our results suggest that the aqueous extract ameliorates 6-OHDA-induced anxiety and depression by attenuation of the oxidative stress in the rat amygdala. These pieces of evidence accentuate its use in traditional medicine.
[Mh] Termos MeSH primário: Albizzia/química
Tonsila do Cerebelo/efeitos dos fármacos
Ansiolíticos/administração & dosagem
Antidepressivos/administração & dosagem
Ansiedade/tratamento farmacológico
Depressão/tratamento farmacológico
Extratos Vegetais/administração & dosagem
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/enzimologia
Tonsila do Cerebelo/metabolismo
Animais
Ansiedade/induzido quimicamente
Ansiedade/metabolismo
Depressão/induzido quimicamente
Depressão/metabolismo
Glutationa Peroxidase/metabolismo
Seres Humanos
Hidroxidopaminas/efeitos adversos
Masculino
Malondialdeído/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Folhas de Planta/química
Ratos
Ratos Wistar
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antidepressive Agents); 0 (Hydroxydopamines); 0 (Plant Extracts); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151021
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-015-0912-0


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[PMID]:26470491
[Au] Autor:Timofeeva MR; Lukina SA
[Ti] Título:[NON-RESPIRATORY FUNCTION OF THE LUNGS IN THE NIGROSTRIATAL DOPAMINERGIC SYSTEM DYSFUNCTION].
[So] Source:Ross Fiziol Zh Im I M Sechenova;101(6):721-30, 2015 Jun.
[Is] ISSN:0869-8139
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The study presents a comprehensive of the metabolism and the fractional composition of li- pids surfactant, water balance, hemostatic activity of the lungs in neyrodegeneration substantia nigra of the brain induced by stereotaxic microinjection of 6--hydroxydopamine and systemic administration of haloperidol. It is shown that a breach of dopaminergic neurotransmission leads to deterioration of surface-active properties of the alveolar lining of the complex against a decrea- se of phospholipids, cholesterol, phosphatidylcholine and lysophospholipids enhance the pulmo- nary surfactant in the activation of phospholipase hydrolysis and lipid peroxidation. Intranigral introduction neurotoxin accompanied by increased blood supply to the lungs and the blood coagu- lation potential of the pulmonary circulation, the blockade D2-receptors--hyporhydration lung tissue. The results obtained indicate the formation of dysregulation pneumopathy dysfunction nigrostriatal dopaminergic system.
[Mh] Termos MeSH primário: Antagonistas de Dopamina/efeitos adversos
Haloperidol/efeitos adversos
Hidroxidopaminas/efeitos adversos
Pulmão
Substância Negra
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antagonistas de Dopamina/farmacologia
Haloperidol/farmacologia
Hidroxidopaminas/farmacologia
Pulmão/metabolismo
Pulmão/patologia
Pulmão/fisiopatologia
Masculino
Ratos
Substância Negra/metabolismo
Substância Negra/patologia
Substância Negra/fisiopatologia
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Antagonists); 0 (Hydroxydopamines); J6292F8L3D (Haloperidol)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:161020
[Lr] Data última revisão:
161020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151017
[St] Status:MEDLINE


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[PMID]:25280422
[Au] Autor:Antunes MS; Goes AT; Boeira SP; Prigol M; Jesse CR
[Ad] Endereço:Laboratório de avaliações farmacológicas e toxicológicas aplicadas às moléculas bioativas-LaftamBio Pampa-Universidade Federal do Pampa, Itaqui, RS, Brazil.
[Ti] Título:Protective effect of hesperidin in a model of Parkinson's disease induced by 6-hydroxydopamine in aged mice.
[So] Source:Nutrition;30(11-12):1415-22, 2014 Nov-Dec.
[Is] ISSN:1873-1244
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Parkinson's disease (PD) may be caused by the interaction of a number of factors, including genetics, toxins, oxidative stress, mitochondrial abnormalities, and aging. Studies have shown that consumption of an antioxidant-rich diet may reduce the incidence of neurodegenerative diseases. The aim of this study was to evaluate the role of the flavonoid hesperidin in an animal model of PD induced by 6-hidroxidopamine (6-OHDA). METHODS: Aged mice were treated with hesperidin (50 mg/kg) during 28 d after an intracerebroventricular injection of 6-OHDA. The enzymatic activities of superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and glutathione S-transferase, the levels of glutathione, reactive oxygen species, total reactive antioxidant potential, dopamine and its levels of metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid, was analyzed in the striatum. The behavioral parameters (depressive-like, memory, and locomotor) were measured. RESULTS: This study demonstrated that hesperidin (50 mg/kg) treatment was effective in preventing memory impairment in the Morris water maze test, as well as, depressive-like behavior in the tail suspension test. Hesperidin attenuated the 6-OHDA-induced reduction in glutathione peroxidase and catalase activity, total reactive antioxidant potential and the dopamine and its metabolite levels in the striatum of aged mice. 6-OHDA increased reactive oxygen species levels and glutathione reductase activity in the striatum, and these alterations were mitigated by chronic administration of hesperidin. CONCLUSION: This study demonstrated a protective effect of hesperidin on the neurotoxicity induced by 6-OHDA in aged mice, indicating that it could be useful as a therapy for the treatment of PD.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Encéfalo/efeitos dos fármacos
Depressão/tratamento farmacológico
Hesperidina/uso terapêutico
Transtornos da Memória/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Antioxidantes/farmacologia
Encéfalo/metabolismo
Depressão/etiologia
Modelos Animais de Doenças
Dopamina/metabolismo
Feminino
Hesperidina/farmacologia
Elevação dos Membros Posteriores
Hidroxidopaminas
Peroxidação de Lipídeos/efeitos dos fármacos
Aprendizagem em Labirinto
Memória/efeitos dos fármacos
Transtornos da Memória/etiologia
Camundongos Endogâmicos C57BL
Doença de Parkinson/complicações
Doença de Parkinson/metabolismo
Fitoterapia
Extratos Vegetais/farmacologia
Extratos Vegetais/uso terapêutico
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Hydroxydopamines); 0 (Plant Extracts); 0 (Reactive Oxygen Species); E750O06Y6O (Hesperidin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:141004
[Lr] Data última revisão:
141004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141005
[St] Status:MEDLINE


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[PMID]:24989117
[Au] Autor:De Luca MA; Cauli O; Morelli M; Simola N
[Ad] Endereço:Department of Biomedical Sciences, Section of Neuropsychopharmacology, University of Cagliari, Cagliari, Italy; National Institute of Neuroscience (INN), University of Cagliari, Cagliari, Italy.
[Ti] Título:Elevation of striatal urate in experimental models of Parkinson's disease: a compensatory mechanism triggered by dopaminergic nigrostriatal degeneration?
[So] Source:J Neurochem;131(3):284-9, 2014 Nov.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Epidemiological studies have indicated an inverse association between high uricemia and incidence of Parkinson's disease (PD). To investigate the link between endogenous urate and neurotoxic changes involving the dopaminergic nigrostriatal system, this study evaluated the modifications in the striatal urate levels in two models of PD. To this end, a partial dopaminergic degeneration was induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice, while a severe dopaminergic degeneration was elicited by unilateral medial forebrain bundle infusion of 6-hydroxydopamine (6-OHDA) in rats. Urate levels were measured by in vivo microdialysis at 7 or 14 days from toxin exposure. The results obtained demonstrated higher urate levels in the dopamine-denervated striatum of 6-OHDA-lesioned rats compared with the intact striatum. Moreover, an inverse correlation between urate and dopamine levels was observed in the same area. In contrast, only a trend to significant increase in striatal urate was observed in MPTP-treated mice. These results demonstrate that a damage to the dopaminergic nigrostriatal system elevates the striatal levels of urate, and suggest that this could be an endogenous compensatory mechanism to attenuate dopaminergic neurodegeneration. This finding may be important in light of the epidemiological and preclinical evidences that indicate a link between urate and development of PD.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/patologia
Intoxicação por MPTP/metabolismo
Neostriado/metabolismo
Neostriado/patologia
Doença de Parkinson Secundária/metabolismo
Substância Negra/metabolismo
Substância Negra/patologia
Ácido Úrico/metabolismo
[Mh] Termos MeSH secundário: Animais
Dopamina/metabolismo
Hidroxidopaminas
Intoxicação por MPTP/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Doença de Parkinson Secundária/induzido quimicamente
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxydopamines); 268B43MJ25 (Uric Acid); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:141021
[Lr] Data última revisão:
141021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140704
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.12809


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[PMID]:24939444
[Au] Autor:Qi C; Xu M; Gan J; Yang X; Wu N; Song L; Yuan W; Liu Z
[Ad] Endereço:Department of Neurology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.
[Ti] Título:Erythropoietin improves neurobehavior by reducing dopaminergic neuron loss in a 6­hydroxydopamine­induced rat model.
[So] Source:Int J Mol Med;34(2):440-50, 2014 Aug.
[Is] ISSN:1791-244X
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to determine the effectiveness of the systemic administration of high dose erythropoietin (EPO) in a 6­hydroxydopamine (6­OHDA)­ induced rat model. Rats were divided into 7 groups. Groups 1­4 were administered daily EPO doses of 0; 2,500; 5,000 and 10,000 U/kg via intraperitoneal injection (i.p.) for 5 days. The EPO concentration in cerebrospinal fluid (CSF) was determined by enzyme­linked immunosorbent assay (ELISA) and western blot analysis. The dose of 10,000 U/kg was then selected for subsequent experiments. In group 5, rats received saline via medial forebrain bundle (MFB). In group 6, rats received 6­OHDA via MFB. In group 7, an EPO concentration of 10,000 U/kg was constantly administered i.p. for 5 days to rats prior to 6­OHDA injection via MFB. Behavioral analysis was performed for groups 5­7 by rat rotation tests. The number of tyrosine hydroxylase (TH)­immunopositive cells in the substantia nigra (SN) was measured by immuno-cyto-chemistry. The activation of c­Jun N­terminal kinase (JNK), extracellular signal­regulated kinase (ERK), p38 mitogen­activated protein kinases (MAPKs) and caspase­3 signaling in rats were analyzed using western blotting. The results showed that there was a significant increase in EPO levels in the CSF in 10,000 U/kg group compared with the 2,500 and 5,000 U/kg groups (P<0.01). Significantly fewer rotational counts were obtained in rats that were pretreated with EPO compared with saline­pretreated 6­OHDA­lesioned rats (P<0.001). The dopaminergic neurons in the 6­OHDA­lesioned SN were also increased in the EPO­pretreated rats when compared with control rats (P<0.01). Western blot analysis revealed that EPO inhibited the 6­OHDA­induced activation of JNK, ERK, p38 MAPK and caspase­3 signaling in the rat model. In conclusion, systemic administration of a high dose of EPO exerted neuroprotective effects in reversing behavioral deficits associated with Parkinson's disease and prevented loss of the dopaminergic neurons through the MAPK pathway.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/efeitos dos fármacos
Eritropoetina/administração & dosagem
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Doença de Parkinson/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Neurônios Dopaminérgicos/patologia
Seres Humanos
Hidroxidopaminas/toxicidade
Fármacos Neuroprotetores
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
Ratos
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxydopamines); 0 (Neuroprotective Agents); 11096-26-7 (Erythropoietin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:150805
[Lr] Data última revisão:
150805
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140619
[St] Status:MEDLINE
[do] DOI:10.3892/ijmm.2014.1810


  10 / 4631 MEDLINE  
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[PMID]:24553948
[Au] Autor:Won L; Ding Y; Singh P; Kang UJ
[Ad] Endereço:Department of Neurology, The University of Chicago, Chicago, Illinois 60637, and Department of Neurology, Columbia University, New York, New York 10032.
[Ti] Título:Striatal cholinergic cell ablation attenuates L-DOPA induced dyskinesia in Parkinsonian mice.
[So] Source:J Neurosci;34(8):3090-4, 2014 Feb 19.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side effect of long-term dopamine replacement therapy in Parkinson's Disease. At present, there are few therapeutic options for treatment of LID and mechanisms contributing to the development and maintenance of these drug-induced motor complications are not well understood. We have previously shown that pharmacological reduction of cholinergic tone attenuates the expression of LID in parkinsonian mice with established dyskinesia after chronic L-DOPA treatment. The present study was undertaken to provide anatomically specific evidence for the role of striatal cholinergic interneurons by ablating them before initiation of L-DOPA treatment and determining whether it decreases LID. We used a novel approach to ablate striatal cholinergic interneurons (ChIs) via Cre-dependent viral expression of the diphtheria toxin A subunit (DT-A) in hemiparkinsonian transgenic mice expressing Cre recombinase under control of the choline acetyltransferase promoter. We show that Cre recombinase-mediated DT-A ablation selectively eliminated ChIs when injected into striatum. The depletion of ChIs markedly attenuated LID without compromising the therapeutic efficacy of L-DOPA. These results provide evidence that ChIs play a key and selective role in LID and that strategies to reduce striatal cholinergic tone may represent a promising approach to decreasing L-DOPA-induced motor complications in Parkinson's disease.
[Mh] Termos MeSH primário: Antiparkinsonianos/toxicidade
Discinesia Induzida por Medicamentos/terapia
Levodopa/toxicidade
Neostriado/fisiologia
Sistema Nervoso Parassimpático/fisiologia
Transtornos Parkinsonianos/terapia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Animais
Comportamento Animal/efeitos dos fármacos
DNA Complementar/biossíntese
DNA Complementar/genética
Denervação
Toxina Diftérica/farmacologia
Discinesia Induzida por Medicamentos/fisiopatologia
Hidroxidopaminas/toxicidade
Processamento de Imagem Assistida por Computador
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neostriado/citologia
Sistema Nervoso Parassimpático/citologia
Transtornos Parkinsonianos/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (DNA, Complementary); 0 (Diphtheria Toxin); 0 (Hydroxydopamines); 46627O600J (Levodopa)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140221
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2888-13.2014



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