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[PMID]:27771535
[Au] Autor:Sim Y; Park G; Eo H; Huh E; Gu PS; Hong SP; Pak YK; Oh MS
[Ad] Endereço:Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
[Ti] Título:Protective effects of a herbal extract combination of Bupleurum falcatum, Paeonia suffruticosa, and Angelica dahurica against MPTP-induced neurotoxicity via regulation of nuclear receptor-related 1 protein.
[So] Source:Neuroscience;340:166-175, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is one of the progressive neurodegenerative diseases of whose condition is characterized by dopaminergic neuronal cell loss and dysfunction in the substantia nigra pars compacta (SNpc) and the striatum. Recent studies have demonstrated that the nuclear receptor-related 1 protein (Nurr1) is critical of dopaminergic phenotype induction in mesencephalic dopaminergic neurons. Further, Nurr1 engages in synthesizing and storing dopamine through regulating levels of tyrosine hydroxylase (TH), dopamine transporter (DAT) and vesicular monoamine transporter 2 (VMAT2). The aim of this study was to investigate the protective effects of a herbal extract combination, consisting of Bupleurum falcatum, Paeonia suffruticosa, and Angelica dahurica (MABH), on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD-like symptoms and to elucidate possible mechanisms of action focusing on Nurr1. In a subacute mouse model of MPTP-induced PD, MABH treatment resulted in recovery from movement impairments. MABH prevented dopamine depletion and protected against dopaminergic neuronal degradation induced by MPTP. Additionally, MABH increased Nurr1 expression in the SNpc of mice. To evaluate the effects of MABH on Nurr1 expression, we measured the protein levels of Nurr1 and its regulating factors using Western blot analysis in PC12 cells. MABH treatment induced the phosphorylation of extracellular signal-regulated kinase protein via increasing the protein expression levels of Nurr1 and ultimately the levels of TH, VMAT2, and DAT. These results indicate that MABH has protective effects on dopaminergic neurons in a mouse model of PD by regulating Nurr1.
[Mh] Termos MeSH primário: Angelica
Bupleurum
Intoxicação por MPTP/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Paeonia
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Animais
Dopamina/metabolismo
Expressão Gênica/efeitos dos fármacos
Intoxicação por MPTP/metabolismo
Intoxicação por MPTP/patologia
Masculino
Camundongos Endogâmicos C57BL
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurônios/patologia
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Células PC12
Parte Compacta da Substância Negra/efeitos dos fármacos
Parte Compacta da Substância Negra/metabolismo
Parte Compacta da Substância Negra/patologia
Fitoterapia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Nr4a2 protein, mouse); 0 (Nr4a2 protein, rat); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Plant Extracts); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171224
[Lr] Data última revisão:
171224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28609288
[Au] Autor:Osacka J; Horvathova L; Majercikova Z; Kiss A
[Ad] Endereço:.
[Ti] Título:Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning.
[So] Source:Endocr Regul;51(2):73-83, 2017 Apr 25.
[Is] ISSN:1210-0668
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Fos protein expression in catecholamine-synthesizing neurons of the substantia nigra (SN) pars compacta (SNC, A8), pars reticulata (SNR, A9), and pars lateralis (SNL), the ventral tegmental area (VTA, A10), the locus coeruleus (LC, A6) and subcoeruleus (sLC), the ventrolateral pons (PON-A5), the nucleus of the solitary tract (NTS-A2), the area postrema (AP), and the ventrolateral medulla (VLM-A1) was quantitatively evaluated aft er a single administration of asenapine (ASE) (designated for schizophrenia treatment) in male Wistar rats preconditioned with a chronic unpredictable variable mild stress (CMS) for 21 days. Th e aim of the present study was to reveal whether a single ASE treatment may 1) activate Fos expression in the brain areas selected; 2) activate tyrosine hydroxylase (TH)-synthesizing cells displaying Fos presence; and 3) be modulated by CMS preconditioning. METHODS: Control (CON), ASE, CMS, and CMS+ASE groups were used. CMS included restraint, social isolation, crowding, swimming, and cold. Th e ASE and CMS+ASE groups received a single dose of ASE (0.3 mg/kg, s.c.) and CON and CMS saline (300 µl/rat, s.c.). The animals were sacrificed 90 min aft er the treatments. Fos protein and TH-labeled immunoreactive perikarya were analyzed on double labeled histological sections and enumerated on captured pictures using combined light and fluorescence microscope illumination. RESULTS: Saline or CMS alone did not promote Fos expression in any of the structures investigated. ASE alone or in combination with CMS elicited Fos expression in two parts of the SN (SNC, SNR) and the VTA. Aside from some cells in the central gray tegmental nuclei adjacent to LC, where a small number of Fos profiles occurred, none or negligible Fos occurrence was detected in the other structures investigated including the LC and sLC, PON-A5, NTS-A2, AP, and VLM-A1. CMS preconditioning did not infl uence the level of Fos induction in the SN and VTA elicited by ASE administration. Similarly, the ratio between the amount of free Fos and Fos colocalized with TH was not aff ected by stress preconditioning in the SNC, SNR, and the VTA. CONCLUSIONS: Th e present study provides an anatomical/functional knowledge about the nature of the acute ASE treatment on the catecholamine-synthesizing neurons activity in certain brain structures and their missing interplay with the CMS preconditioning.
[Mh] Termos MeSH primário: Antipsicóticos/farmacologia
Encéfalo/efeitos dos fármacos
Condicionamento (Psicologia)
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Neurônios/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/efeitos dos fármacos
Estresse Psicológico/metabolismo
Tirosina 3-Mono-Oxigenase/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Área Postrema/citologia
Área Postrema/efeitos dos fármacos
Área Postrema/metabolismo
Encéfalo/citologia
Encéfalo/metabolismo
Catecolaminas/biossíntese
Imuno-Histoquímica
Locus Cerúleo/citologia
Locus Cerúleo/efeitos dos fármacos
Locus Cerúleo/metabolismo
Masculino
Bulbo/citologia
Bulbo/efeitos dos fármacos
Bulbo/metabolismo
Microscopia de Fluorescência
Neurônios/metabolismo
Parte Compacta da Substância Negra/citologia
Parte Compacta da Substância Negra/efeitos dos fármacos
Parte Compacta da Substância Negra/metabolismo
Parte Reticular da Substância Negra/citologia
Parte Reticular da Substância Negra/efeitos dos fármacos
Parte Reticular da Substância Negra/metabolismo
Ponte/citologia
Ponte/efeitos dos fármacos
Ponte/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Wistar
Núcleo Solitário/citologia
Núcleo Solitário/efeitos dos fármacos
Núcleo Solitário/metabolismo
Estresse Psicológico/psicologia
Tirosina 3-Mono-Oxigenase/metabolismo
Área Tegmentar Ventral/citologia
Área Tegmentar Ventral/efeitos dos fármacos
Área Tegmentar Ventral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Catecholamines); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Proto-Oncogene Proteins c-fos); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); JKZ19V908O (Asenapine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


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[PMID]:28303260
[Au] Autor:Voutilainen MH; De Lorenzo F; Stepanova P; Bäck S; Yu LY; Lindholm P; Pörsti E; Saarma M; Männistö PT; Tuominen RK
[Ad] Endereço:Division of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikki Biocenter, University of Helsinki, FIN-00014 Helsinki, Finland; Institute of Biotechnology, Viikki Biocenter, University of Helsinki, FIN-00014 Helsinki, Finland.
[Ti] Título:Evidence for an Additive Neurorestorative Effect of Simultaneously Administered CDNF and GDNF in Hemiparkinsonian Rats: Implications for Different Mechanism of Action.
[So] Source:eNeuro;4(1), 2017 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a neurodegenerative disorder associated with a progressive loss of dopaminergic (DAergic) neurons of the substantia nigra (SN) and the accumulation of intracellular inclusions containing α-synuclein. Current therapies do not stop the progression of the disease, and the efficacy of these treatments wanes over time. Neurotrophic factors (NTFs) are naturally occurring proteins promoting the survival and differentiation of neurons and the maintenance of neuronal contacts. CDNF (cerebral dopamine NTF) and GDNF (glial cell line-derived NTF) are able to protect DAergic neurons against toxin-induced degeneration in experimental models of PD. Here, we report an additive neurorestorative effect of coadministration of CDNF and GDNF in the unilateral 6-hydroxydopamine (6-OHDA) lesion model of PD in rats. NTFs were given into the striatum four weeks after unilateral intrastriatal injection of 6-OHDA (20 µg). Amphetamine-induced (2.5 mg/kg, i.p.) rotational behavior was measured every two weeks. Number of tyrosine hydroxylase (TH)-positive cells from SN pars compacta (SNpc) and density of TH-positive fibers in the striatum were analyzed at 12 weeks after lesion. CDNF and GDNF alone restored the DAergic function, and one specific dose combination had an additive effect: CDNF (2.5µg) and GDNF (1µg) coadministration led to a stronger trophic effect relative to either of the single treatments alone. The additive effect may indicate different mechanism of action for the NTFs. Indeed, both NTFs activated the survival promoting PI3 kinase (PI3K)-Akt signaling pathway, but only CDNF decreased the expression level of tested endoplasmatic reticulum (ER) stress markers ATF6, glucose-regulated protein 78 (GRP78), and phosphorylation of eukaryotic initiation factor 2α subunit (eIF2α).
[Mh] Termos MeSH primário: Antiparkinsonianos/administração & dosagem
Fator Neurotrófico Derivado de Linhagem de Célula Glial/administração & dosagem
Fatores de Crescimento Neural/administração & dosagem
Transtornos Parkinsonianos/tratamento farmacológico
[Mh] Termos MeSH secundário: Anfetamina/farmacologia
Animais
Células Cultivadas
Estimulantes do Sistema Nervoso Central/farmacologia
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/metabolismo
Corpo Estriado/patologia
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/metabolismo
Neurônios Dopaminérgicos/patologia
Sinergismo Farmacológico
Quimioterapia Combinada
Lateralidade Funcional
Masculino
Camundongos
Atividade Motora/efeitos dos fármacos
Fármacos Neuroprotetores/administração & dosagem
Oxidopamina
Transtornos Parkinsonianos/metabolismo
Transtornos Parkinsonianos/patologia
Parte Compacta da Substância Negra/efeitos dos fármacos
Parte Compacta da Substância Negra/metabolismo
Parte Compacta da Substância Negra/patologia
Ratos Wistar
Proteínas Recombinantes/administração & dosagem
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (CDNF protein, human); 0 (Central Nervous System Stimulants); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Nerve Growth Factors); 0 (Neuroprotective Agents); 0 (Recombinant Proteins); 8HW4YBZ748 (Oxidopamine); CK833KGX7E (Amphetamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


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[PMID]:28238669
[Au] Autor:Baluchnejadmojarad T; Rabiee N; Zabihnejad S; Roghani M
[Ad] Endereço:Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: tmojarad@yahoo.com.
[Ti] Título:Ellagic acid exerts protective effect in intrastriatal 6-hydroxydopamine rat model of Parkinson's disease: Possible involvement of ERß/Nrf2/HO-1 signaling.
[So] Source:Brain Res;1662:23-30, 2017 May 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a prevalent movement disorder in the elderly with progressive loss of mesencephalic dopaminergic neurons and incapacitating motor and non-motor complications. Ellagic acid is a natural phenolic compound with potent antioxidant and anti-inflammatory properties. In this study, we investigated its possible neuroprotective effect in 6-hydroxydopamine (6-OHDA) rat model of PD. Intrastriatal 6-OHDA-lesioned rats were pretreated with ellagic acid at a dose of 50mg/kg/day for 1week. Results showed that ellagic acid attenuates apomorphine-induced rotational bias and lowers the latency to initiate and the total time in the narrow beam task and this beneficial effect was partially abrogated following intracerebroventricular microinjection of estrogen receptor ß (ERß) antagonist. Furthermore, ellagic acid reduced striatal malondialdehyde (MDA), reactive oxygen species (ROS), and DNA fragmentation, and improved monoamine oxidase B (MAO-B), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and heme oxygenase 1 (HO-1). Meanwhile, ellagic acid prevented loss of tyrosine hydroxylase (TH)-positive neurons within substantia nigra pars compacta (SNC). These findings indicate neuroprotective potential of ellagic acid in 6-OHDA rat model of PD via amelioration of apoptosis and oxidative stress, suppression of MAO-B, and its favorable influence is partly reliant on ERß/Nrf2/HO-1 signaling cascade.
[Mh] Termos MeSH primário: Ácido Elágico/metabolismo
Ácido Elágico/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Corpo Estriado/metabolismo
Neurônios Dopaminérgicos/metabolismo
Receptor beta de Estrogênio/antagonistas & inibidores
Heme Oxigenase (Desciclizante)
Malondialdeído
Modelos Animais
Monoaminoxidase
Fator 2 Relacionado a NF-E2
Neostriado/metabolismo
Fármacos Neuroprotetores/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
Oxidopamina/farmacologia
Doença de Parkinson/tratamento farmacológico
Parte Compacta da Substância Negra/metabolismo
Ratos
Espécies Reativas de Oxigênio
Transdução de Sinais/efeitos dos fármacos
Substância Negra/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Estrogen Receptor beta); 0 (NF-E2-Related Factor 2); 0 (Neuroprotective Agents); 0 (Nfe2l2 protein, rat); 0 (Reactive Oxygen Species); 19YRN3ZS9P (Ellagic Acid); 4Y8F71G49Q (Malondialdehyde); 8HW4YBZ748 (Oxidopamine); EC 1.14.14.18 (Heme Oxygenase (Decyclizing)); EC 1.14.14.18 (Hmox1 protein, rat); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE


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[PMID]:28233992
[Au] Autor:Herrera A; Muñoz P; Steinbusch HWM; Segura-Aguilar J
[Ad] Endereço:Molecular & Clinical Pharmacology, ICBM, Faculty of Medicine, University of Chile , Santiago, Chile.
[Ti] Título:Are Dopamine Oxidation Metabolites Involved in the Loss of Dopaminergic Neurons in the Nigrostriatal System in Parkinson's Disease?
[So] Source:ACS Chem Neurosci;8(4):702-711, 2017 Apr 19.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In 1967, L-dopa was introduced as part of the pharmacological therapy of Parkinson's disease (PD) and, in spite of extensive research, no additional effective drugs have been discovered to treat PD. This brings forward the question: why have no new drugs been developed? We consider that one of the problems preventing the discovery of new drugs is that we still have no information on the pathophysiology of the neurodegeneration of the neuromelanin-containing nigrostriatal dopaminergic neurons. Currently, it is widely accepted that the degeneration of dopaminergic neurons, i.e., in the substantia nigra pars compacta, involves mitochondrial dysfunction, the formation of neurotoxic oligomers of alpha-synuclein, the dysfunction of protein degradation systems, neuroinflammation, and oxidative and endoplasmic reticulum stress. However, the initial trigger of these mechanisms in the nigrostriatal system is still unknown. It has been reported that aminochrome induces the majority of these mechanisms involved in the neurodegeneration process. Aminochrome is formed within the cytoplasm of neuromelanin-containing dopaminergic neurons during the oxidation of dopamine to neuromelanin. The oxidation of dopamine to neuromelanin is a normal and harmless process, because healthy individuals have intact neuromelanin-containing dopaminergic neurons. Interestingly, aminochrome-induced neurotoxicity is prevented by two enzymes: DT-diaphorase and glutathione transferase M2-2, which explains why melanin-containing dopaminergic neurons are intact in healthy human brains.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Neurônios Dopaminérgicos/patologia
Degeneração Neural/metabolismo
Doença de Parkinson/patologia
Parte Compacta da Substância Negra/patologia
[Mh] Termos MeSH secundário: Animais
Neurônios Dopaminérgicos/metabolismo
Seres Humanos
Melaninas/metabolismo
Degeneração Neural/fisiopatologia
Oxirredução
Doença de Parkinson/metabolismo
Doença de Parkinson/fisiopatologia
Parte Compacta da Substância Negra/metabolismo
Parte Compacta da Substância Negra/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Melanins); 0 (neuromelanin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.7b00034


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[PMID]:28212832
[Au] Autor:Blanco-Lezcano L; Jimenez-Martin J; Díaz-Hung ML; Alberti-Amador E; Wong-Guerra M; González-Fraguela ME; Estupiñán-Díaz B; Serrano-Sánchez T; Francis-Turner L; Delgado-Ocaña S; Núñez-Figueredo Y; Vega-Hurtado Y; Fernández-Jiménez I
[Ad] Endereço:Experimental Neurophysiology Department, International Center of Neurological Restoration (CIREN), Ave. 25 No. 15805 e/ 158 and 160, Playa, CP: 11300 Havana, Cuba; Latinoamerican School of Medicine, Km 3½ Carretera Panamericana, Santa Fé, Playa, Havana, Cuba. Electronic address: lisette.blanco@infom
[Ti] Título:Motor dysfunction and alterations in glutathione concentration, cholinesterase activity, and BDNF expression in substantia nigra pars compacta in rats with pedunculopontine lesion.
[So] Source:Neuroscience;348:83-97, 2017 Apr 21.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pedunculopontine nucleus (PPN) has been considered a critically important region in the regulation of some of the physiological functions that fail during the progression of Parkinson's disease (PD). In this paper, the effects of unilateral neurotoxic lesion of the PPN [through the injection of N-methyl-d-aspartate (NMDA) solution (concentration: 0.1M; volume: 0.5µL)] in motor execution and gait disorders and the changes in cellular and molecular indicators in rat nigral tissue were evaluated. The motor execution was assessed using the beam test (BT) and the gait disorders by footprint test. Glutathione (GSH) concentrations, acetyl cholinesterase enzymatic activity (AChE EA), and brain-derived neurotrophic factor (BDNF) mRNA expression in nigral tissue were analyzed. NMDA-lesioned rats showed fine motor dysfunction with a significant increase in the slow (p≤0.01) and fast movement (p≤0.01) time and in path deviation (p≤0.01) on the smaller diameter beams. Moreover, NMDA-lesioned rats exhibited an imprecise path with moments of advances and setbacks, alternating with left and right deviations, suspensions, and inverted positions. Footprint test revealed slight gait disorders, which were manifested by a reduction in the left and right stride lengths, the intra-step distance, and the support area (p≤0.01). Biochemical studies showed that 48h after the PPN neurotoxic injury, the GSH concentrations and BDNF expression were significantly increased (p≤0.01). These variables returned to normal values 7days after the PPN lesion; the AChE EA showed a significant increase at this time. These functional changes in nigral tissue could be a plastic responses associated with early PD.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/metabolismo
Colinesterases/metabolismo
Marcha/fisiologia
Glutationa/metabolismo
Parte Compacta da Substância Negra/metabolismo
Núcleo Tegmental Pedunculopontino/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Marcha/efeitos dos fármacos
Masculino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
N-Metilaspartato/toxicidade
Parte Compacta da Substância Negra/fisiopatologia
Núcleo Tegmental Pedunculopontino/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 6384-92-5 (N-Methylaspartate); EC 3.1.1.8 (Cholinesterases); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE


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[PMID]:28153913
[Au] Autor:Jung SY; Choi JM; Rousseaux MW; Malovannaya A; Kim JJ; Kutzera J; Wang Y; Huang Y; Zhu W; Maity S; Zoghbi HY; Qin J
[Ad] Endereço:From the ‡Verna & Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77003; syjung@bcm.edu jqin@bcm.edu.
[Ti] Título:An Anatomically Resolved Mouse Brain Proteome Reveals Parkinson Disease-relevant Pathways.
[So] Source:Mol Cell Proteomics;16(4):581-593, 2017 Apr.
[Is] ISSN:1535-9484
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here, we present a mouse brain protein atlas that covers 17 surgically distinct neuroanatomical regions of the adult mouse brain, each less than 1 mm in size. The protein expression levels are determined for 6,500 to 7,500 gene protein products from each region and over 12,000 gene protein products for the entire brain, documenting the physiological repertoire of mouse brain proteins in an anatomically resolved and comprehensive manner. We explored the utility of our spatially defined protein profiling methods in a mouse model of Parkinson's disease. We compared the proteome from a vulnerable region (substantia nigra pars compacta) of wild type and parkinsonian mice with that of an adjacent, less vulnerable, region (ventral tegmental area) and identified several proteins that exhibited both spatiotemporal- and genotype-restricted changes. We validated the most robustly altered proteins using an alternative profiling method and found that these modifications may highlight potential new pathways for future studies. This proteomic atlas is a valuable resource that offers a practical framework for investigating the molecular intricacies of normal brain function as well as regional vulnerability in neurological diseases. All of the mouse regional proteome profiling data are published on line at http://mbpa.bprc.ac.cn/.
[Mh] Termos MeSH primário: Doença de Parkinson/metabolismo
Parte Compacta da Substância Negra/metabolismo
Proteômica/métodos
Área Tegmentar Ventral/metabolismo
[Mh] Termos MeSH secundário: Animais
Mapeamento Encefálico
Modelos Animais de Doenças
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Proteoma/análise
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proteome)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1074/mcp.M116.061440


  8 / 116 MEDLINE  
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[PMID]:28130746
[Au] Autor:Prajapati SK; Garabadu D; Krishnamurthy S
[Ad] Endereço:Neurotherapeutics Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P, 221 005, India.
[Ti] Título:Coenzyme Q10 Prevents Mitochondrial Dysfunction and Facilitates Pharmacological Activity of Atorvastatin in 6-OHDA Induced Dopaminergic Toxicity in Rats.
[So] Source:Neurotox Res;31(4):478-492, 2017 May.
[Is] ISSN:1476-3524
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atorvastatin (ATV) generally used to treat dyslipidemia is also reported to have effect against 6-hydroxydopamine (6-OHDA) induced neurotoxicity. Additionally, atorvastatin can interfere with mitochondrial function by reducing the level of Q10. Therefore, the therapeutic effect of atorvastatin (20 mg/kg) could be compromised. In this context, the present study evaluated the effect of ATV supplemented with Q10. 6-OHDA was unilaterally injected into the right striatum of male rats. On day 8 of 6-OHDA infusion, ATV (20 mg/kg), Q10 (200 mg/kg), and their combination were administered per oral for 14 days. On day 21, there was significant loss of striatal dopamine indicating neurotoxicity. The combination of ATV+Q10 showed significant amelioration of dopamine (DA) toxicity compared to individual treatments. Similarly, ATV+Q10 compared to individual treatment significantly decreased the motor deficits induced by 6-OHDA. Further, 6-OHDA induced mitochondrial dysfunction in the substantia nigra pars compacta (SNpc). There was significant decrease in mitochondrial complex enzyme activities and mitochondrial membrane potential (MMP). Treatment with ATV and ATV+Q10 ameliorated mitochondrial dysfunction by increasing complex enzyme activities; however, only ATV+Q10 were able to stabilize MMP and maintained mitochondrial integrity. Moreover, there was significant induction of oxidative stress as observed from increase in lipid peroxidases (LPO) and nitrite (NO), and decrease in super oxide dismutase (SOD). Treatment with ATV+Q10 significantly altered the above effects indicating antioxidant activity. Furthermore, only combination of ATV and Q10 decreased the 6-OHDA induced expression of cytochrome-C, caspase-9 and caspase-3. Therefore, current results provide evidence that supplementation of Q10 with ATV shows synergistic effect in reducing dopamine toxicity.
[Mh] Termos MeSH primário: Atorvastatina Cálcica/farmacologia
Neurônios Dopaminérgicos/efeitos dos fármacos
Ubiquinona/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Caspase 3/metabolismo
Caspase 9/metabolismo
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/metabolismo
Dopamina/metabolismo
Sinergismo Farmacológico
Complexo IV da Cadeia de Transporte de Elétrons/metabolismo
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Mitocôndrias/metabolismo
Atividade Motora/efeitos dos fármacos
Destreza Motora/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Oxidopamina
Parte Compacta da Substância Negra/metabolismo
Ubiquinona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 1339-63-5 (Ubiquinone); 48A5M73Z4Q (Atorvastatin Calcium); 8HW4YBZ748 (Oxidopamine); EC 1.9.3.1 (Electron Transport Complex IV); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9); EJ27X76M46 (coenzyme Q10); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE
[do] DOI:10.1007/s12640-016-9693-6


  9 / 116 MEDLINE  
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[PMID]:28038352
[Au] Autor:Richter F; Gabby L; McDowell KA; Mulligan CK; De La Rosa K; Sioshansi PC; Mortazavi F; Cely I; Ackerson LC; Tsan L; Murphy NP; Maidment NT; Chesselet MF
[Ad] Endereço:Department of Neurology, UCLA, Los Angeles, CA, USA. Electronic address: franziska.richter@vmf.uni-leipzig.de.
[Ti] Título:Effects of decreased dopamine transporter levels on nigrostriatal neurons and paraquat/maneb toxicity in mice.
[So] Source:Neurobiol Aging;51:54-66, 2017 Mar.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:How genetic variations in the dopamine transporter (DAT) combined with exposure to environmental toxins modulate the risk of Parkinson's disease remains unclear. Using unbiased stereology in DAT knock-down mice (DAT-KD) and wild-type (WT) littermates, we found that decreased DAT caused a loss of tyrosine hydroxylase-positive (dopaminergic) neurons in subregions of the substantia nigra pars compacta at 3-4 days, 5 weeks, and 18 months of age. Both genotypes lost dopaminergic neurons with age and remaining neurons at 11 months were resilient to paraquat/maneb. In 5-week-old mice, the toxins decreased substantia nigra pars compacta dopaminergic neurons in both genotypes but less in DAT-KD. Regional analysis revealed striking differences in the subsets of neurons affected by low DAT, paraquat/maneb, and aging. In particular, we show that a potentially protective effect of low DAT against toxin exposure is not sufficient to reduce death of all nigrostriatal dopaminergic neurons. Thus, different regional vulnerability of nigrostriatal dopaminergic neurons may contribute to an increased risk of developing Parkinson's disease when multiple factors are combined.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Proteínas da Membrana Plasmática de Transporte de Dopamina/deficiência
Proteínas da Membrana Plasmática de Transporte de Dopamina/genética
Neurônios Dopaminérgicos/patologia
Variação Genética
Maneb/toxicidade
Paraquat/toxicidade
Doença de Parkinson/etiologia
Parte Compacta da Substância Negra/patologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Masculino
Camundongos Knockout
Camundongos Mutantes
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Plasma Membrane Transport Proteins); 12427-38-2 (Maneb); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161231
[St] Status:MEDLINE


  10 / 116 MEDLINE  
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[PMID]:27913104
[Au] Autor:Li Y; Liu W; Li L; Hölscher C
[Ad] Endereço:Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan, Shanxi, PR China; Department of human anatomy, Shaoyang Medical College, Shaoyang, Hunan, PR China.
[Ti] Título:D-Ala2-GIP-glu-PAL is neuroprotective in a chronic Parkinson's disease mouse model and increases BNDF expression while reducing neuroinflammation and lipid peroxidation.
[So] Source:Eur J Pharmacol;797:162-172, 2017 Feb 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Type 2 diabetes mellitus (T2DM) is a risk factor for Parkinson's disease (PD). Therefore, treatment to improve insulin resistance in T2DM may be useful for PD patients. Glucose dependent insulinotropic polypeptide (GIP) is a member of the incretin hormone family that can promote insulin release and improve insulin resistance. Several GIP analogues have been developed as potential treatments for T2DM. We had shown previously that D-Ala2-GIP-glu-PAL, a novel long-acting GIP analogue, can play a neuroprotective role in the PD mouse model induced by acute MPTP injection. The drug reduced damage to the dopaminergic neurons and increased CREB-mediated Bcl-2 expression to prevent apoptosis and reduced chronic inflammation in the brain. In the present study, we further tested the effects of chronic treatment by D-Ala2-GIP-glu-PAL in a chronic PD mouse model induced by MPTP (25mg/kg ip.) combination with probenecid (250mg/kg ip.) injection for 5 weeks. The results demonstrated that chronic treatment with D-Ala2-GIP-glu-PAL inhibits MPTP -induced Parkinsonism-like motor disorders in mice, and that the drug prevents dopaminergic neuronal loss in the substantia nigra pars compacta (SNpc). Moreover, D-Ala2-GIP-glu-PAL also inhibited the increased levels of expression of α-synuclein in the SNpc and striatum induced by MPTP. Furthermore, drug treatment reduced chronic neuroinflammation, oxidative stress and lipid peroxidation, and increased the expression of BDNF. These findings show that GIP signaling is neuroprotective and holds promise as a novel treatment of PD.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/metabolismo
Polipeptídeo Inibidor Gástrico/análogos & derivados
Polipeptídeo Inibidor Gástrico/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Peroxidação de Lipídeos/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
Doença de Parkinson/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Astrócitos/patologia
Contagem de Células
Doença Crônica
Modelos Animais de Doenças
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/patologia
Polipeptídeo Inibidor Gástrico/uso terapêutico
Inflamação/tratamento farmacológico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/efeitos dos fármacos
Microglia/metabolismo
Microglia/patologia
Atividade Motora/efeitos dos fármacos
Neostriado/efeitos dos fármacos
Neostriado/metabolismo
Neostriado/patologia
Doença de Parkinson/patologia
Doença de Parkinson/fisiopatologia
Parte Compacta da Substância Negra/efeitos dos fármacos
Parte Compacta da Substância Negra/metabolismo
Parte Compacta da Substância Negra/patologia
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ala2-GIP-Glu-PAL); 0 (Brain-Derived Neurotrophic Factor); 0 (alpha-Synuclein); 59392-49-3 (Gastric Inhibitory Polypeptide)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170407
[Lr] Data última revisão:
170407
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE



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