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Pesquisa : D02.092.471.683.915 [Categoria DeCS]
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[PMID]:29221756
[Au] Autor:Lesniak A; Aarnio M; Diwakarla S; Norberg T; Nyberg F; Gordh T
[Ad] Endereço:Uppsala University, Department of Pharmaceutical Biosciences, SE 751 24 Uppsala, Sweden; Medical University of Warsaw, Department of Pharmacodynamics, Centre for Preclinical Research and Technology, 02-097 Warsaw, Poland. Electronic address: anna.lesniak@wum.edu.pl.
[Ti] Título:Characterization of the binding site for d-deprenyl in human inflamed synovial membrane.
[So] Source:Life Sci;194:26-33, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: d-Deprenyl when used as a positron emission tomography tracer visualizes peripheral inflammation. The major aim of the current study was to identify and investigate the properties of the binding target for d-deprenyl in synovial membrane explants from arthritic patients. MAIN METHODS: Thirty patients diagnosed with arthritis or osteoarthritis were enrolled into the study. Homologous and competitive radioligand binding assays utilizing [ H]d-deprenyl were performed to investigate the biochemical characteristics of the binding site and assess differences in the binding profile in synovial membranes exhibiting varying levels of inflammation. KEY FINDINGS: The [ H]d-deprenyl binding assay confirmed the existence of a single, saturable population of membrane-bound protein binding sites in synovial membrane homogenates. The macroscopically determined level of inflammation correlated with an increase in [ H]d-deprenyl binding affinity, without significant alterations in binding site density. Selective monoamine oxidase B inhibitor, selegiline competed for the same site as [ H]d-deprenyl, but failed to differentiate the samples with regard to their inflammation grade. A monoamine oxidase A inhibitor, pirlindole mesylate showed only weak displacement of [ H]d-deprenyl binding. No significant alterations in monoamine oxidase B expression was detected, thus it was not confirmed whether it could serve as a marker for ongoing inflammation. SIGNIFICANCE: Our study was the first to show the biochemical characteristics of the [ H]d-deprenyl binding site in inflamed human synovium. We confirmed that d-deprenyl could differentiate between patients with varying severity of synovitis in the knee joint by binding to a protein target distinct from monoamine oxidase B.
[Mh] Termos MeSH primário: Artrite/diagnóstico
Inibidores da Monoaminoxidase/metabolismo
Monoaminoxidase/análise
Selegilina/metabolismo
Membrana Sinovial/patologia
Sinovite/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Artrite/metabolismo
Sítios de Ligação
Feminino
Seres Humanos
Masculino
Meia-Idade
Monoaminoxidase/metabolismo
Tomografia por Emissão de Pósitrons
Ensaio Radioligante
Membrana Sinovial/metabolismo
Sinovite/metabolismo
Trítio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Monoamine Oxidase Inhibitors); 10028-17-8 (Tritium); 2K1V7GP655 (Selegiline); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:28753307
[Au] Autor:Fonseca A; Reis J; Silva T; Matos MJ; Bagetta D; Ortuso F; Alcaro S; Uriarte E; Borges F
[Ad] Endereço:CIQUP/Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto , 4169-007 Porto, Portugal.
[Ti] Título:Coumarin versus Chromone Monoamine Oxidase B Inhibitors: Quo Vadis?
[So] Source:J Med Chem;60(16):7206-7212, 2017 Aug 24.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Because of the lack of significant disease-modifying drugs for neurodegenerative disorders, a pressing need for new chemical entities endowed with IMAO-B still exists. Within this framework, and for the first time, a study was performed to compare coumarin- and chomone-3-phenylcarboxamide scaffolds. Compounds 10a and 10b were the most potent, selective, and reversible noncompetitive IMAO-B. The benzopyrone sp oxygen atom was found to be position independent and a productive contributor for the ligand-enzyme complex stability.
[Mh] Termos MeSH primário: Cromonas/farmacologia
Cumarínicos/farmacologia
Inibidores da Monoaminoxidase/farmacologia
Monoaminoxidase/metabolismo
[Mh] Termos MeSH secundário: Alanina/análogos & derivados
Alanina/farmacologia
Benzilaminas/farmacologia
Cromonas/síntese química
Cromonas/química
Clorgilina/farmacologia
Cumarínicos/síntese química
Cumarínicos/química
Seres Humanos
Indanos/farmacologia
Cinética
Ligantes
Simulação de Acoplamento Molecular
Monoaminoxidase/química
Inibidores da Monoaminoxidase/síntese química
Inibidores da Monoaminoxidase/química
Selegilina/farmacologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylamines); 0 (Chromones); 0 (Coumarins); 0 (Indans); 0 (Ligands); 0 (Monoamine Oxidase Inhibitors); 0 (N-(3-chlorophenyl)-6-methylchromone-3-carboxamide); 0 (N-(3-chlorophenyl)-6-methylcoumarin-3-carboxamide); 003N66TS6T (rasagiline); 2K1V7GP655 (Selegiline); 90ENL74SIG (safinamide); EC 1.4.3.4 (Monoamine Oxidase); EC 1.4.3.4. (monoamine oxidase A, human); LYJ16FZU9Q (Clorgyline); OF5P57N2ZX (Alanine)
[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:170729
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00918


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[PMID]:28623006
[Au] Autor:Knoll J; Baghy K; Eckhardt S; Ferdinandy P; Garami M; Harsing LG; Hauser P; Mervai Z; Pocza T; Schaff Z; Schuler D; Miklya I
[Ad] Endereço:Department of Pharmacology and Pharmacotherapy, Faculty of Medicine in Semmelweis University, Budapest, Hungary. Electronic address: knoll.jozsef@med.semmelweis-univ.hu.
[Ti] Título:A longevity study with enhancer substances (selegiline, BPAP) detected an unknown tumor-manifestation-suppressing regulation in rat brain.
[So] Source:Life Sci;182:57-64, 2017 Aug 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: First proof to show that (-)-deprenyl/selegiline (DEP), the first selective inhibitor of MAO-B, later identified as the first ß-phenylethylamine (PEA)-derived synthetic catecholaminergic activity enhancer (CAE) substance and (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine (BPAP), the tryptamine-derived presently known most potent, selective, synthetic enhancer substance, are specific markers of unknown enhancer-sensitive brain regulations. MAIN METHODS: Longevity study disclosing the operation of tumor-manifestation-suppressing (TMS) regulation in rat brain. Immonohistochemical identification of a fibromyxosarcoma in rats. Experiments with human medulloblastoma cell lines. Analysis of the mechanism of action of enhancer substances. KEY FINDINGS: Whereas 20/40 saline-treated rats manifested a fibromyxosarcoma, in groups of rats treated with 0.001mg/kg DEP: 15/40 rats; with 0.1mg/kg DEP: 11/40 rats (P<0.01); with 0.0001mg/kg BPAP: 8/40 rats (P<0.001); with 0.05mg/kg BPAP: 7/40 rats (P<0.01) manifested the tumor. Experiments with human medulloblastoma cell lines, HTB-186 (Daoy); UW-228-2, showed that BPAP was devoid of direct cytotoxic effect on tumor cells, and did not alter the direct cytotoxic effectiveness of temozolomide, cisplatin, etoposide, or vincristine. Interaction with distinct sites on vesicular monoamine-transporter-2 (VMAT2) is the main mechanism of action of the enhancer substances which clarifies the highly characteristic bi-modal, bell-shaped concentration-effect curves of DEP and BPAP. SIGNIFICANCE: Considering of the safeness of the enhancer substances and the finding that DEP and BPAP, specific markers of unknown enhancer sensitive brain regulations, detected the operation of an enhancer-sensitive TMS-regulation in rat brain, it seems reasonable to test in humans low dose DEP or BPAP treatment against the spreading of a malignant tumor.
[Mh] Termos MeSH primário: Benzofuranos/farmacologia
Encéfalo/efeitos dos fármacos
Longevidade/efeitos dos fármacos
Inibidores da Monoaminoxidase/farmacologia
Selegilina/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Benzofuranos/administração & dosagem
Encéfalo/metabolismo
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Fibrossarcoma/prevenção & controle
Seres Humanos
Masculino
Meduloblastoma/tratamento farmacológico
Inibidores da Monoaminoxidase/administração & dosagem
Ratos
Ratos Wistar
Selegilina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-(benzofuran-2-yl)-2-propylaminopentane); 0 (Antineoplastic Agents); 0 (Benzofurans); 0 (Monoamine Oxidase Inhibitors); 2K1V7GP655 (Selegiline)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170618
[St] Status:MEDLINE


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[PMID]:28359327
[Au] Autor:Ng KP; Pascoal TA; Mathotaarachchi S; Therriault J; Kang MS; Shin M; Guiot MC; Guo Q; Harada R; Comley RA; Massarweh G; Soucy JP; Okamura N; Gauthier S; Rosa-Neto P
[Ad] Endereço:Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, 6825 LaSalle Boulevard, Verdun, Québec, H4H 1R3, Canada.
[Ti] Título:Monoamine oxidase B inhibitor, selegiline, reduces F-THK5351 uptake in the human brain.
[So] Source:Alzheimers Res Ther;9(1):25, 2017 Mar 31.
[Is] ISSN:1758-9193
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: F-THK5351 is a quinoline-derived tau imaging agent with high affinity to paired helical filaments (PHF). However, high levels of F-THK5351 retention in brain regions thought to contain negligible concentrations of PHF raise questions about the interpretation of the positron emission tomography (PET) signals, particularly given previously described interactions between quinolone derivatives and monoamine oxidase B (MAO-B). Here, we tested the effects of MAO-B inhibition on F-THK5351 brain uptake using PET and autoradiography. METHODS: Eight participants (five mild cognitive impairment, two Alzheimer's disease, and one progressive supranuclear palsy) had baseline F-AZD4694 and F-THK5351 scans in order to quantify brain amyloid and PHF load, respectively. A second F-THK5351 scan was conducted 1 week later, 1 h after a 10-mg oral dose of selegiline. Three out of eight patients also had a third F-THK5351 scan 9-28 days after the selegiline administration. The primary outcome measure was standardized uptake value (SUV), calculated using tissue radioactivity concentration from 50 to 70 min after F-THK5351 injection, normalizing for body weight and injected radioactivity. The SUV ratio (SUVR) was determined using the cerebellar cortex as the reference region. F-THK5351 competition autoradiography studies in postmortem tissue were conducted using 150 and 500 nM selegiline. RESULTS: At baseline, F-THK5351 SUVs were highest in the basal ganglia (0.64 ± 0.11) and thalamus (0.62 ± 0.14). In the post-selegiline scans, the regional SUVs were reduced on average by 36.7% to 51.8%, with the greatest reduction noted in the thalamus (51.8%) and basal ganglia (51.4%). MAO-B inhibition also reduced F-THK5351 SUVs in the cerebellar cortex (41.6%). The SUVs remained reduced in the three patients imaged at 9-28 days. Tissue autoradiography confirmed the effects of MAO-B inhibition on F-THK5351 uptake. CONCLUSIONS: These results indicate that the interpretation of F-THK5351 PET images, with respect to tau, is confounded by the high MAO-B availability across the entire brain. In addition, the heterogeneous MAO-B availability across the cortex may limit the interpretation of F-THK5351 scans using reference region methods.
[Mh] Termos MeSH primário: Aminopiridinas/farmacocinética
Encéfalo/diagnóstico por imagem
Radioisótopos de Flúor/farmacocinética
Inibidores da Monoaminoxidase/farmacologia
Monoaminoxidase/metabolismo
Quinolinas/farmacocinética
Selegilina/farmacologia
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/diagnóstico por imagem
Doença de Alzheimer/metabolismo
Autorradiografia
Ligação Competitiva
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Disfunção Cognitiva/diagnóstico por imagem
Disfunção Cognitiva/metabolismo
Interações Medicamentosas
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos
Paralisia Supranuclear Progressiva/diagnóstico por imagem
Paralisia Supranuclear Progressiva/metabolismo
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminopyridines); 0 (Fluorine Radioisotopes); 0 (MAPT protein, human); 0 (Monoamine Oxidase Inhibitors); 0 (Quinolines); 0 (Radiopharmaceuticals); 0 (THK5351); 0 (tau Proteins); 2K1V7GP655 (Selegiline); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1186/s13195-017-0253-y


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[PMID]:28276259
[Au] Autor:Liu B; Lv C; Zhang J; Liu Y; Sun J; Cheng X; Mao W; Ma Y; Li S
[Ad] Endereço:a First Department of Neurology , Hospital Affiliated to North China University of Science and Technology , Tangshan , China.
[Ti] Título:Effects of eldepryl on glial cell proliferation and activation in the substantia nigra and striatum in a rat model of Parkinson's disease.
[So] Source:Neurol Res;39(5):459-467, 2017 May.
[Is] ISSN:1743-1328
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Inflammation is involved in the occurrence and progression of Parkinson's disease (PD), but the exact mechanisms remain unclear. This study aimed to observe the expressions of glial fibrillary acidic protein (GFAP) and integrin αM (CD11b) in the substantia nigra and striatum, and to investigate the effect of eldepryl on these expressions in a rat model of PD. METHODS: Seventy-two rats were randomly divided into three groups: control, model, and eldepryl. Each group was randomly divided into 4-day and 8-day subgroups (n = 12 rats/group) after successful establishment of the model. The rat model of PD was established by subcutaneous injection of rotenone through the back of the neck. After model establishment, the rats were given physiological saline in the control and model groups, and eldepryl in the eldepryl group for 4 or 8 days. The numbers of GFAP-positive and CD11b-positive cells and expressions of GFAP and CD11b were detected by immunohistochemistry and western blotting analysis, respectively. RESULTS: GFAP-positive and CD11b-positive cells changed from their normal quiescent state into a so-called reactive state. GFAP and CD11b expressions were upregulated in the substantia nigra and striatum in the model group compared with the control group (p < 0.05), but there were no significant differences between 8 and 4 days (p > 0.05). In the eldepryl group, GFAP and CD11b expressions were decreased compared with the model group (p < 0.05), with a significant decrease for 8 days compared with 4 days (p < 0.05). DISCUSSION: Glial cells were greatly proliferated and activated in the substantia nigra and striatum of rats with PD, and eldepryl could prevent the progression of PD by inhibiting the proliferation and activation of glial cells.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Corpo Estriado/patologia
Neuroglia/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
Selegilina/uso terapêutico
Substância Negra/patologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Antígeno CD11b/metabolismo
Proliferação Celular/fisiologia
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Masculino
Doença de Parkinson/patologia
Ratos
Ratos Sprague-Dawley
Selegilina/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Glial Fibrillary Acidic Protein); 2K1V7GP655 (Selegiline)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/01616412.2017.1297911


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[PMID]:28108387
[Au] Autor:Cui Y; Liu KW; Liang Y; Ip MS; Mak JC
[Ad] Endereço:Department of Medicine, The University of Hong Kong, Hong Kong.
[Ti] Título:Inhibition of monoamine oxidase-B by selegiline reduces cigarette smoke-induced oxidative stress and inflammation in airway epithelial cells.
[So] Source:Toxicol Lett;268:44-50, 2017 Feb 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic obstructive pulmonary disease (COPD) is caused by the build-up of oxidative stress-induced damages due to cigarette smoking, but how monoamine oxidase (MAO)-B signaling is involved remains unclear. This study aims to establish the involvement of MAO-B signaling pathways in cigarette smoke medium (CSM)-induced oxidative stress and inflammation in human airway epithelial cells (AECs). CSM treatment increased MAO-B activity, ROS levels and IL-8 release in AECs. Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner. Selegiline also reversed CSM-induced changes of anti-oxidant enzymes superoxide dismutase (SOD) and catalase (CAT) activities, GSH/GSSG ratio, as well expression of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1). The effects of selegiline are partially driven through the nuclear factor erythroid 2 related factor 2 (Nrf2) and cytosol translocation of its negative regulator, BTB and CNC homolog 1 (Bach1). Nevertheless, selegiline fully reversed the CSM-induced effects on IKK, cytoplasmic IκB expression, and nuclear translocation of nuclear factor-κB (NF-κB) p65 subunit. Our study demonstrated that in AECs, inhibition of MAO-B using selegiline reversed the CSM-induced oxidative stress and inflammation. These data may provide a novel strategy for therapy in COPD.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Antioxidantes/farmacologia
Brônquios/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Inibidores da Monoaminoxidase/farmacologia
Monoaminoxidase/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Pneumonia/prevenção & controle
Selegilina/farmacologia
Fumaça/efeitos adversos
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Brônquios/enzimologia
Brônquios/patologia
Linhagem Celular
Citoproteção
Relação Dose-Resposta a Droga
Células Epiteliais/enzimologia
Células Epiteliais/patologia
Seres Humanos
Mediadores da Inflamação/metabolismo
Interleucina-8/metabolismo
NF-kappa B/metabolismo
Pneumonia/enzimologia
Pneumonia/patologia
Doença Pulmonar Obstrutiva Crônica/enzimologia
Doença Pulmonar Obstrutiva Crônica/patologia
Doença Pulmonar Obstrutiva Crônica/prevenção & controle
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (IL8 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-8); 0 (Monoamine Oxidase Inhibitors); 0 (NF-kappa B); 0 (Reactive Oxygen Species); 0 (Smoke); 2K1V7GP655 (Selegiline); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE


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[PMID]:28013042
[Au] Autor:Shirzad H; Esmaeili F; Bakhshalizadeh S; Ebrahimie M; Ebrahimie E
[Ad] Endereço:Cellular & Molecular Research Center, Shahrekord University of Medical Sciences, PO Box 8815713471, Shahrekord, Iran. Electronic address: shirzadeh@yahoo.com.
[Ti] Título:Production of stable GFP-expressing neural cells from P19 embryonal carcinoma stem cells.
[So] Source:Mol Cell Probes;32:46-54, 2017 Apr.
[Is] ISSN:1096-1194
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Murine P19 embryonal carcinoma (EC) cells are convenient to differentiate into all germ layer derivatives. One of the advantages of P19 cells is that the exogenous DNA can be easily inserted into them. Here, at the first part of this study, we generated stable GFP-expressing P19 cells (P19-GFP ). FACS and western-blot analysis confirmed stable expression of GFP in the cells. We previously demonstrated the efficient induction of neuronal differentiation from mouse ES and EC cells by application of a neuroprotective drug, selegiline In the second part of this study selegiline was used to induce differentiation of P19-GFP into stable GFP-expressing neuron-like cells. Cresyl violet staining confirmed neuronal morphology of the differentiated cells. Furthermore, real-time PCR and immunoflourescence approved the expression of neuron specific markers. P19-GFP cells were able to survive, migrate and integrated into host tissues when transplanted to developing chick embryo CNS. The obtained live GFP-expressing cells can be used as an abundant source of developmentally pluripotent material for transplantation studies, investigating the cellular and molecular aspects of early differentiation.
[Mh] Termos MeSH primário: Técnicas de Cultura de Células/métodos
Células-Tronco de Carcinoma Embrionário/patologia
Proteínas de Fluorescência Verde/metabolismo
Neurônios/metabolismo
Neurônios/patologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Galinhas
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
Células-Tronco de Carcinoma Embrionário/transplante
Fluorescência
Imunofluorescência
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Camundongos
Neurônios/efeitos dos fármacos
Selegilina/farmacologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
147336-22-9 (Green Fluorescent Proteins); 2K1V7GP655 (Selegiline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161226
[St] Status:MEDLINE


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[PMID]:27901472
[Au] Autor:Lalkovicova M; Horvathova F; Sulla I; Mihalik J; Danielisova V
[Ad] Endereço:Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia. lalkovicova@saske.sk.
[Ti] Título:Effects of low and high deprenyl dose on antioxidant enzyme activities in the adult rat brain.
[So] Source:Gen Physiol Biophys;36(1):83-90, 2017 Jan.
[Is] ISSN:0231-5882
[Cp] País de publicação:Slovakia
[La] Idioma:eng
[Ab] Resumo:We evaluated the effects of low dose deprenyl (LDD, 0.0025 mg/kg per day) and high dose deprenyl (HDD, 0.25 mg/kg per day) treatment of male Wistar rats for 30 days on the activities of SOD and CAT in the cortex, striatum, and hippocampus. Total SOD and MnSOD activities were increased with LDD (p <0.05) in the cortex (0.74 ± 0.03; 0.31 ± 0.02), striatum (0.75 ± 0.02; 0.27 ± 0.03) and CA1 region of the hippocampus (0.75 ± 0.02; 0.29 ± 0.03) compared to the control (0.53 ± 0.02; 0.15 ± 0.02), but reduced (p <0.05) with HDD compared to the LDD group. CAT activity was increased (p <0.05) with LDD in the cortex (27.34 ± 3.11), striatum (22.22 ± 1.85), and hippocampal CA1 region (16.62 ± 2.15) compared to control (10.33 ± 1.01), while a decrease was induced by HDD in the striatum (9.85 ± 1.09) compared to LDD. There was a significant (p <0.05) difference in number of Fluoro Jade B positive CA1 neurons induced by LDD (21.14 ± 2.85%) and HDD (12.61 ± 1.42%), as well as the number of NeuN positive CA1 neurons after LDD (183.35 ± 11.14 cells/mm) and HDD (238.45 ± 14.11 cells/mm (p < 0.05). Deprenyl showed a potential in improving the neurological outcome and reducing the oxidative damage.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Encéfalo/efeitos dos fármacos
Encéfalo/enzimologia
Catalase/metabolismo
Selegilina/farmacologia
Superóxido Dismutase/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Inibidores da Monoaminoxidase/farmacologia
Ratos
Ratos Wistar
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Monoamine Oxidase Inhibitors); 2K1V7GP655 (Selegiline); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.4149/gpb_2016023


  9 / 2280 MEDLINE  
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[PMID]:27984094
[Au] Autor:Bundgaard C; Montezinho LP; Anderson N; Thomsen C; Mørk A
[Ad] Endereço:H. Lundbeck A/S, Neuroscience Research, 9 Ottiliavej, DK-2500 Copenhagen-Valby, Denmark. Electronic address: cbun@lundbeck.com.
[Ti] Título:Selegiline induces a wake promoting effect in rats which is related to formation of its active metabolites.
[So] Source:Pharmacol Biochem Behav;150-151:147-152, 2016 Nov - Dec.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The goal of the present work was to characterise the effects of selegiline on the rat sleep pattern. Furthermore, for comparative purposes, the pharmacokinetics of selegiline and its metabolites in brain and plasma were investigated, and microdialysis experiments were performed to examine the resulting effect on dopamine, noradrenaline and serotonin levels. Selegiline (1, 5, 10 and 30mg/kg) was found to dose-dependently increase the time spent awake following acute dosing. The pharmacokinetic assessment of selegiline showed that, following an oral dose of 5mg/kg, low circulating levels of the parent compound were found relative to those of biotransformed l-methamphetamine and l-amphetamine. The time course of selegiline-induced wakefulness was shown to follow the time course of l-methamphetamine and l-amphetamine in brain, suggesting that these metabolites are responsible for the modulation of sleep architecture. Furthermore, selegiline (5mg/kg) caused a significant increase of extracellular levels of DA (250%) and NA (200%), but not of 5-HT, in the rat prefrontal cortex. In summary, an integrated experimental approach was undertaken here to evaluate selegiline's effect on sleep architecture in rats in relation to its pharmacokinetics and changes in monoaminergic neurotransmitter levels in the brain. The effect of selegiline on sleep was likely mediated by an increase of dopamine and noradrenaline levels in the brain caused by the formed metabolites.
[Mh] Termos MeSH primário: Inibidores da Monoaminoxidase/farmacologia
Selegilina/farmacologia
Vigília/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Biotransformação
Dopamina/análise
Relação Dose-Resposta a Droga
Masculino
Microdiálise
Norepinefrina/análise
Córtex Pré-Frontal/química
Ratos
Ratos Sprague-Dawley
Selegilina/metabolismo
Sono/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Monoamine Oxidase Inhibitors); 2K1V7GP655 (Selegiline); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


  10 / 2280 MEDLINE  
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[PMID]:27861613
[Au] Autor:Popova D; Forsblad A; Hashemian S; Jacobsson SO
[Ad] Endereço:Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
[Ti] Título:Non-Serotonergic Neurotoxicity by MDMA (Ecstasy) in Neurons Derived from Mouse P19 Embryonal Carcinoma Cells.
[So] Source:PLoS One;11(11):e0166750, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:3,4-methylenedioxymethamphetamine (MDMA; ecstasy) is a commonly abused recreational drug that causes neurotoxic effects in both humans and animals. The mechanism behind MDMA-induced neurotoxicity is suggested to be species-dependent and needs to be further investigated on the cellular level. In this study, the effects of MDMA in neuronally differentiated P19 mouse embryonal carcinoma cells have been examined. MDMA produces a concentration-, time- and temperature-dependent toxicity in differentiated P19 neurons, as measured by intracellular MTT reduction and extracellular LDH activity assays. The P19-derived neurons express both the serotonin reuptake transporter (SERT), that is functionally active, and the serotonin metabolizing enzyme monoamine oxidase A (MAO-A). The involvement of these proteins in the MDMA-induced toxicity was investigated by a pharmacological approach. The MAO inhibitors clorgyline and deprenyl, and the SERT inhibitor fluoxetine, per se or in combination, were not able to mimic the toxic effects of MDMA in the P19-derived neurons or block the MDMA-induced cell toxicity. Oxidative stress has been implicated in MDMA-induced neurotoxicity, but pre-treatment with the antioxidants α-tocopherol or N-acetylcysteine did not reveal any protective effects in the P19 neurons. Involvement of mitochondria in the MDMA-induced cytotoxicity was also examined, but MDMA did not alter the mitochondrial membrane potential (ΔΨm) in the P19 neurons. We conclude that MDMA produce a concentration-, time- and temperature-dependent neurotoxicity and our results suggest that the mechanism behind MDMA-induced toxicity in mouse-derived neurons do not involve the serotonergic system, oxidative stress or mitochondrial dysfunction.
[Mh] Termos MeSH primário: N-Metil-3,4-Metilenodioxianfetamina/farmacologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Clorgilina/farmacologia
Células-Tronco de Carcinoma Embrionário
Fluoxetina/farmacologia
Expressão Gênica
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Monoaminoxidase/genética
Monoaminoxidase/metabolismo
Selegilina/farmacologia
Proteínas da Membrana Plasmática de Transporte de Serotonina/genética
Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Serotonin Plasma Membrane Transport Proteins); 01K63SUP8D (Fluoxetine); 2K1V7GP655 (Selegiline); EC 1.4.3.4 (Monoamine Oxidase); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine); LYJ16FZU9Q (Clorgyline)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166750



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