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[PMID]:29200326
[Au] Autor:Bartlett R; Stokes L; Curtis SJ; Curtis BL; Sluyter R
[Ad] Endereço:a School of Biological Sciences, University of Wollongong , Wollongong , NSW , Australia.
[Ti] Título:Probenecid directly impairs activation of the canine P2X7 receptor.
[So] Source:Nucleosides Nucleotides Nucleic Acids;36(12):736-744, 2017 Dec 02.
[Is] ISSN:1532-2335
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The current study aimed to determine if probenecid could directly impair the canine P2X7 receptor, a ligand-gated cation channel activated by extracellular adenosine 5'-triphosphate (ATP). Patch clamp measurements demonstrated that probenecid impairs ATP-induced inward currents in HEK-293 cells expressing canine P2X7. Flow cytometric measurements of ethidium uptake into HEK-293 cells expressing canine P2X7 showed that probenecid impairs ATP-induced pore formation in a concentration-dependent manner, with a half maximal inhibitory concentration of 158 µM. Finally, ELISA measurements revealed that probenecid impairs ATP-induced interleukin-1ß release in dog blood. In conclusion, this study reveals that probenecid can directly impair canine P2X7 activation.
[Mh] Termos MeSH primário: Probenecid/farmacologia
Antagonistas do Receptor Purinérgico P2X/farmacologia
Receptores Purinérgicos P2X7/metabolismo
[Mh] Termos MeSH secundário: Animais
Cães
Células HEK293
Seres Humanos
Interleucina-1beta/secreção
Porosidade
Receptores Purinérgicos P2X7/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Purinergic P2X Receptor Antagonists); 0 (Receptors, Purinergic P2X7); PO572Z7917 (Probenecid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1080/15257770.2017.1391395


  2 / 3114 MEDLINE  
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[PMID]:28953988
[Au] Autor:Wang YH; Ke XM; Zhang CH; Yang RP
[Ad] Endereço:Chongqing Academy of Chinese Materia Medica, Chongqing, China.
[Ti] Título:Absorption mechanism of three curcumin constituents through in situ intestinal perfusion method.
[So] Source:Braz J Med Biol Res;50(11):e6353, 2017 Sep 21.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate the absorption mechanism of three curcumin constituents in rat small intestines. Self-emulsification was used to solubilize the three curcumin constituents, and the rat in situ intestinal perfusion method was used to study factors on drug absorption, including drug mass concentration, absorption site, and the different types and concentrations of absorption inhibitors. Within the scope of experimental concentrations, three curcumin constituents were absorbed in rat small intestines through the active transport mechanism.
[Mh] Termos MeSH primário: Adjuvantes Farmacêuticos/farmacologia
Curcumina/análogos & derivados
Curcumina/farmacocinética
Inibidores Enzimáticos/farmacocinética
Absorção Intestinal
Intestino Delgado/metabolismo
[Mh] Termos MeSH secundário: 2,4-Dinitrofenol/farmacocinética
Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores
Animais
Cromatografia Líquida de Alta Pressão/métodos
Curcumina/química
Emulsões
Feminino
Absorção Intestinal/efeitos dos fármacos
Intestino Delgado/efeitos dos fármacos
Masculino
Proteínas Associadas à Resistência a Múltiplos Medicamentos/análise
Proteínas Associadas à Resistência a Múltiplos Medicamentos/antagonistas & inibidores
Imagem de Perfusão/métodos
Probenecid/farmacologia
Ratos Sprague-Dawley
Valores de Referência
Reprodutibilidade dos Testes
Fatores de Tempo
Desacopladores/farmacologia
Verapamil/farmacologia
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abcc2 protein, rat); 0 (Adjuvants, Pharmaceutic); 0 (Emulsions); 0 (Enzyme Inhibitors); 0 (Multidrug Resistance-Associated Proteins); 0 (Uncoupling Agents); 2EFO1BP34R (bis(4-hydroxycinnamoyl)methane); 4AF605U6JN (multidrug resistance-associated protein 2); CJ0O37KU29 (Verapamil); IT942ZTH98 (Curcumin); PO572Z7917 (Probenecid); Q13SKS21MN (2,4-Dinitrophenol); W2F8059T80 (demethoxycurcumin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


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[PMID]:28912345
[Au] Autor:Zhang QS; Heng Y; Chen Y; Luo P; Wen L; Zhang Z; Yuan YH; Chen NH
[Ad] Endereço:State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica and Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Q.-S.Z., Y.H., Y.C., L.W., Z.Z., Y.-H.Y., N.-H.C.); and College of Pharmacy, Hun
[Ti] Título:A Novel Bibenzyl Compound (20C) Protects Mice from 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine/Probenecid Toxicity by Regulating the -Synuclein-Related Inflammatory Response.
[So] Source:J Pharmacol Exp Ther;363(2):284-292, 2017 Nov.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The novel bibenzyl compound 2-[4-hydroxy-3-(4- hydroxyphenyl) benzyl]-4-(4- hydroxyphenyl) phenol (20C) plays a neuroprotective role in vitro, but its effects in vivo have not yet been elucidated. In this study, we estimated the efficacy of 20C in vivo using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/p) mouse model from behavior, dopamine, and neuron and then the possible mechanisms for these effects were further investigated. The experimental results showed that 20C improved behavioral deficits, attenuated dopamine depletion, reduced dopaminergic neuron loss, protected the blood-brain barrier (BBB) structure, ameliorated -synuclein dysfunction, suppressed glial activation, and regulated both nuclear factor- B (NF- B) signaling and the NOD-like receptor protein (NLRP) 3 inflammasome pathway. Our results indicated that 20C may prevent neurodegeneration in the MPTP/p mouse model by targeting -synuclein and regulating -synuclein-related inflammatory responses, including BBB damage, glial activation, NF- B signaling, and the NLRP3 inflammasome pathway.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Bibenzilas/farmacologia
Intoxicação por MPTP/prevenção & controle
Fármacos Neuroprotetores/farmacologia
Fenóis/farmacologia
Probenecid/toxicidade
[Mh] Termos MeSH secundário: Animais
Astrócitos/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Dopamina/metabolismo
Inflamação/metabolismo
Intoxicação por MPTP/metabolismo
Intoxicação por MPTP/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/efeitos dos fármacos
NF-kappa B/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3-(4-hydroxybenzyl)-4-hydroxybenzyl)-4-(4-hydroxybenzyl)phenol); 0 (Benzhydryl Compounds); 0 (Bibenzyls); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Neuroprotective Agents); 0 (Phenols); PO572Z7917 (Probenecid); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.244020


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[PMID]:28686657
[Au] Autor:Clark RSB; Empey PE; Bayir H; Rosario BL; Poloyac SM; Kochanek PM; Nolin TD; Au AK; Horvat CM; Wisniewski SR; Bell MJ
[Ad] Endereço:Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
[Ti] Título:Phase I randomized clinical trial of N-acetylcysteine in combination with an adjuvant probenecid for treatment of severe traumatic brain injury in children.
[So] Source:PLoS One;12(7):e0180280, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There are no therapies shown to improve outcome after severe traumatic brain injury (TBI) in humans, a leading cause of morbidity and mortality. We sought to verify brain exposure of the systemically administered antioxidant N-acetylcysteine (NAC) and the synergistic adjuvant probenecid, and identify adverse effects of this drug combination after severe TBI in children. METHODS: IRB-approved, randomized, double-blind, placebo controlled Phase I study in children 2 to 18 years-of-age admitted to a Pediatric Intensive Care Unit after severe TBI (Glasgow Coma Scale [GCS] score ≤8) requiring an externalized ventricular drain for measurement of intracranial pressure (ICP). Patients were recruited from November 2011-August 2013. Fourteen patients (n = 7/group) were randomly assigned after obtaining informed consent to receive probenecid (25 mg/kg load, then 10 mg/kg/dose q6h×11 doses) and NAC (140 mg/kg load, then 70 mg/kg/dose q4h×17 doses), or placebos via naso/orogastric tube. Serum and CSF samples were drawn pre-bolus and 1-96 h after randomization and drug concentrations were measured via UPLC-MS/MS. Glasgow Outcome Scale (GOS) score was assessed at 3 months. RESULTS: There were no adverse events attributable to drug treatment. One patient in the placebo group was withdrawn due to adverse effects. In the treatment group, NAC concentrations ranged from 16,977.3±2,212.3 to 16,786.1±3,285.3 in serum and from 269.3±113.0 to 467.9±262.7 ng/mL in CSF, at 24 to 72 h post-bolus, respectively; and probenecid concentrations ranged from 75.4.3±10.0 to 52.9±25.8 in serum and 5.4±1.0 to 4.6±2.1 µg/mL in CSF, at 24 to 72 h post-bolus, respectively (mean±SEM). Temperature, mean arterial pressure, ICP, use of ICP-directed therapies, surveillance serum brain injury biomarkers, and GOS at 3 months were not different between groups. CONCLUSIONS: Treatment resulted in detectable concentrations of NAC and probenecid in CSF and was not associated with undesirable effects after TBI in children. TRIAL REGISTRATION: ClinicalTrials.gov NCT01322009.
[Mh] Termos MeSH primário: Acetilcisteína/farmacocinética
Adjuvantes Farmacêuticos/farmacocinética
Antioxidantes/farmacocinética
Lesões Encefálicas Traumáticas/tratamento farmacológico
Probenecid/farmacocinética
[Mh] Termos MeSH secundário: Acetilcisteína/sangue
Acetilcisteína/líquido cefalorraquidiano
Acetilcisteína/farmacologia
Adjuvantes Farmacêuticos/farmacologia
Adolescente
Antioxidantes/farmacologia
Biomarcadores/sangue
Temperatura Corporal
Lesões Encefálicas Traumáticas/sangue
Lesões Encefálicas Traumáticas/líquido cefalorraquidiano
Lesões Encefálicas Traumáticas/mortalidade
Criança
Pré-Escolar
Método Duplo-Cego
Esquema de Medicação
Feminino
Escala de Coma de Glasgow
Escala de Resultado de Glasgow
Seres Humanos
Pressão Intracraniana/efeitos dos fármacos
Intubação Gastrointestinal
Masculino
Probenecid/sangue
Probenecid/líquido cefalorraquidiano
Probenecid/farmacologia
Análise de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Adjuvants, Pharmaceutic); 0 (Antioxidants); 0 (Biomarkers); PO572Z7917 (Probenecid); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180280


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[PMID]:28587784
[Au] Autor:Flores K; Manautou JE; Renfro JL
[Ad] Endereço:Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.
[Ti] Título:Gender-specific expression of ATP-binding cassette (Abc) transporters and cytoprotective genes in mouse choroid plexus.
[So] Source:Toxicology;386:84-92, 2017 Jul 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The choroid plexus (CP) and blood-brain barrier (BBB) control the movement of several drugs and endogenous compounds between the brain and systemic circulation. The multidrug resistance associated protein (Mrp) efflux transporters form part of these barriers. Several Mrp transporters are positively regulated by the transcription factor nuclear factor erythroid-2-related factor (Nrf2) in liver. The Mrps, Nrf2 and Nrf2-dependent genes are cytoprotective and our aim was to examine basal gender differences in expression of Mrp transporters, Nrf2 and Nrf2-dependent genes (Nqo1 and Ho-1) in the brain-barriers. Previous studies have shown higher expression of Mrp1, Mrp2 and Mrp4 in female mouse liver and kidney. We hypothesized that similar renal/hepatic gender-specific patterns are present in the brain-barrier epithelia interfaces. qPCR and immunoblot analyses showed that Mrp4, Ho-1 and Nqo1 expression was higher in female CP. Mrp1, Mrp2 and Nrf2 expression in the CP had no gender pattern. Female Mrp1, Mrp2 and Mrp4 mouse brain expressions in remaining brain areas, excluding CP, were higher than male. Functional analysis of Mrp4 in CP revealed active accumulation of the Mrp4 model substrate fluo-cAMP. WT female CP had 10-fold higher accumulation in the vascular spaces than males and 60% higher than Mrp4 females. Probenecid blocked all transport. Methotrexate did as well except in Mrp4 females where it had no effect, suggesting compensatory induction of transport occurred in Mrp4 . Collectively, our findings indicate significant gender differences in expression of Mrp transporters and cytoprotective genes in the CP and BBB.
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/genética
Barreira Hematoencefálica/metabolismo
Plexo Corióideo/metabolismo
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Regulação da Expressão Gênica
Rim/metabolismo
Fígado/metabolismo
Masculino
Metotrexato/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fator 2 Relacionado a NF-E2/metabolismo
Probenecid/farmacologia
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abcc4 protein, mouse); 0 (Multidrug Resistance-Associated Proteins); 0 (NF-E2-Related Factor 2); PO572Z7917 (Probenecid); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  6 / 3114 MEDLINE  
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[PMID]:28472795
[Au] Autor:Favretto G; Souza LM; Gregório PC; Cunha RS; Maciel RAP; Sassaki GL; Toledo MG; Pecoits-Filho R; Souza WM; Stinghen AEM
[Ad] Endereço:Experimental Nephrology Laboratory, Basic Pathology Department, Universidade Federal do Paraná, Curitiba, Brazil.
[Ti] Título:Role of Organic Anion Transporters in the Uptake of Protein-Bound Uremic Toxins by Human Endothelial Cells and Monocyte Chemoattractant Protein-1 Expression.
[So] Source:J Vasc Res;54(3):170-179, 2017.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Organic anion transporters (OATs) are involved in the uptake of uremic toxins such as p-cresyl sulfate (PCS) and indoxyl sulfate (IS), which play a role in endothelial dysfunction in patients with chronic kidney diseases (CKD). In this study, we investigated the role of OAT1 and OAT3 in the uptake of PCS and IS into human endothelial cells. PCS was synthesized via p-cresol sulfation and characterized using analytical methods. The cells were treated with PCS and IS in the absence and presence of probenecid (Pb), an OAT inhibitor. Cell viability was assessed using the MTT assay. The absorbed toxins were analyzed using chromatography, OAT expression using immunocytochemistry and western blot, and monocyte chemoattractant protein-1 (MCP-1) expression using enzyme-linked immunosorbent assay. Cell viability decreased after toxin treatment in a dose-dependent manner. PCS and IS showed significant internalization after 60 min treatment, while no internalization was observed in the presence of Pb, suggesting that OATs are involved in the transport of both toxins. Immunocytochemistry and western blot demonstrated OAT1 and OAT3 expression in endothelial cells. MCP-1 expression increased after toxins treatment but decreased after Pb treatment. PCS and IS uptake were mediated by OATs, and OAT blockage could serve as a therapeutic strategy to inhibit MCP-1 expression.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Células Endoteliais/metabolismo
Proteína 1 Transportadora de Ânions Orgânicos/metabolismo
Transportadores de Ânions Orgânicos Sódio-Independentes/metabolismo
Uremia/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Cresóis/metabolismo
Cresóis/toxicidade
Relação Dose-Resposta a Droga
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/patologia
Seres Humanos
Indicã/metabolismo
Indicã/toxicidade
Proteína 1 Transportadora de Ânions Orgânicos/antagonistas & inibidores
Transportadores de Ânions Orgânicos Sódio-Independentes/antagonistas & inibidores
Probenecid/farmacologia
Ésteres do Ácido Sulfúrico/metabolismo
Ésteres do Ácido Sulfúrico/toxicidade
Fatores de Tempo
Regulação para Cima
Uremia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cresols); 0 (Organic Anion Transport Protein 1); 0 (Organic Anion Transporters, Sodium-Independent); 0 (Sulfuric Acid Esters); 0 (organic anion transport protein 3); 56M34ZQY1S (4-cresol sulfate); N187WK1Y1J (Indican); PO572Z7917 (Probenecid)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1159/000468542


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[PMID]:28192112
[Au] Autor:Römermann K; Fedrowitz M; Hampel P; Kaczmarek E; Töllner K; Erker T; Sweet DH; Löscher W
[Ad] Endereço:Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Germany.
[Ti] Título:Multiple blood-brain barrier transport mechanisms limit bumetanide accumulation, and therapeutic potential, in the mammalian brain.
[So] Source:Neuropharmacology;117:182-194, 2017 May 01.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:There is accumulating evidence that bumetanide, which has been used over decades as a potent loop diuretic, also exerts effects on brain disorders, including autism, neonatal seizures, and epilepsy, which are not related to its effects on the kidney but rather mediated by inhibition of the neuronal Na-K-Cl cotransporter isoform NKCC1. However, following systemic administration, brain levels of bumetanide are typically below those needed to inhibit NKCC1, which critically limits its clinical use for treating brain disorders. Recently, active efflux transport at the blood-brain barrier (BBB) has been suggested as a process involved in the low brain:plasma ratio of bumetanide, but it is presently not clear which transporters are involved. Understanding the processes explaining the poor brain penetration of bumetanide is needed for developing strategies to improve the brain delivery of this drug. In the present study, we administered probenecid and more selective inhibitors of active transport carriers at the BBB directly into the brain of mice to minimize the contribution of peripheral effects on the brain penetration of bumetanide. Furthermore, in vitro experiments with mouse organic anion transporter 3 (Oat3)-overexpressing Chinese hamster ovary cells were performed to study the interaction of bumetanide, bumetanide derivatives, and several known inhibitors of Oats on Oat3-mediated transport. The in vivo experiments demonstrated that the uptake and efflux of bumetanide at the BBB is much more complex than previously thought. It seems that both restricted passive diffusion and active efflux transport, mediated by Oat3 but also organic anion-transporting polypeptide (Oatp) Oatp1a4 and multidrug resistance protein 4 explain the extremely low brain concentrations that are achieved after systemic administration of bumetanide, limiting the use of this drug for targeting abnormal expression of neuronal NKCC1 in brain diseases.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/fisiologia
Encéfalo/metabolismo
Bumetanida/farmacocinética
Proteínas Associadas à Resistência a Múltiplos Medicamentos/fisiologia
Transportadores de Ânions Orgânicos Sódio-Independentes/fisiologia
Proteínas de Transporte de Cátions Orgânicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/efeitos dos fármacos
Barreira Hematoencefálica/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Bumetanida/análogos & derivados
Células CHO
Células Cultivadas
Cricetinae
Cricetulus
Difusão
Feminino
Moduladores de Transporte de Membrana/farmacologia
Camundongos
Transportadores de Ânions Orgânicos/antagonistas & inibidores
Transportadores de Ânions Orgânicos/genética
Transportadores de Ânions Orgânicos Sódio-Independentes/antagonistas & inibidores
Transportadores de Ânions Orgânicos Sódio-Independentes/metabolismo
Probenecid/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abcc4 protein, mouse); 0 (Membrane Transport Modulators); 0 (Multidrug Resistance-Associated Proteins); 0 (Oatp2 protein, mouse); 0 (Organic Anion Transporters); 0 (Organic Anion Transporters, Sodium-Independent); 0 (Organic Cation Transport Proteins); 0 (organic anion transport protein 3); 0Y2S3XUQ5H (Bumetanide); PO572Z7917 (Probenecid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE


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[PMID]:28185878
[Au] Autor:Janakiraman U; Manivasagam T; Justin Thenmozhi A; Dhanalakshmi C; Essa MM; Song BJ; Guillemin GJ
[Ad] Endereço:Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, 608002, Tamilnadu, India.
[Ti] Título:Chronic mild stress augments MPTP induced neurotoxicity in a murine model of Parkinson's disease.
[So] Source:Physiol Behav;173:132-143, 2017 May 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Depression is frequently encountered during Parkinson's disease (PD) as a non-motor feature, which has been reported to cause and exaggerate motor deficits and neurodegenerative events in experimental PD models. We studied the effect of chronic mild stress (CMS) (pre, post and pre & post) exposure mediated depression on motor and non-motor symptoms, oxidative stress, inflammation and brain derived neurotrophic factor (BDNF) levels and its related signalling molecules against the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/p) induced neurotoxicity in mice. CMS and MPTP/p-coexposed C57BL/6 mice exhibited low neuromuscular strength and stride length with enhanced oxidative stress and inflammation as compared to CMS or MPTP/p alone exposed mice. Coexposure diminished the levels of BDNF and expressions of p-TrkB, p-ERK/ERK, p-AKT/AKT and p-CREB in nigrostriatal regions as compared to those of the alone exposure. CMS alone exposed mice showed more anxiety related behaviour with diminished expression of serotonin transporter as compared to MPTP/p alone injected group. Post-stress exposure to MPTP/p mice exhibited lowest motor and reflecting higher anxiety state with greatest enhancement in inflammation and reduction in the protein expression of stress and cell signalling markers as compared to pre and pre & post stress exposed PD mice. However, pre- and pre & post CMS exposed PD animals are more vulnerable to oxidative stress as compared with post-stress experienced MPTP/p mice. CMS mediated depression exacerbates motor/non-motor symptoms in MPTP/p-PD animals by modulating oxidative stress and various signalling molecules. Our results suggested that stress induced NMS can accelerate neurodegenerative processes in the PD in a progressive or expedited manner.
[Mh] Termos MeSH primário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/efeitos adversos
Transtornos Parkinsonianos/fisiopatologia
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Adjuvantes Farmacêuticos/toxicidade
Animais
Peso Corporal/efeitos dos fármacos
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Catalase/metabolismo
Modelos Animais de Doenças
Comportamento Exploratório/efeitos dos fármacos
Proteína Glial Fibrilar Ácida/metabolismo
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas dos Microfilamentos/metabolismo
Força Muscular/efeitos dos fármacos
Probenecid/toxicidade
Transdução de Sinais/efeitos dos fármacos
Superóxido Dismutase/metabolismo
Tiobarbitúricos/toxicidade
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Pharmaceutic); 0 (Aif1 protein, rat); 0 (Brain-Derived Neurotrophic Factor); 0 (Calcium-Binding Proteins); 0 (Glial Fibrillary Acidic Protein); 0 (Microfilament Proteins); 0 (Thiobarbiturates); 0 (Thiobarbituric Acid Reactive Substances); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); M1YZW5SS7C (thiobarbituric acid); PO572Z7917 (Probenecid)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE


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[PMID]:28134928
[Au] Autor:Burma NE; Bonin RP; Leduc-Pessah H; Baimel C; Cairncross ZF; Mousseau M; Shankara JV; Stemkowski PL; Baimoukhametova D; Bains JS; Antle MC; Zamponi GW; Cahill CM; Borgland SL; De Koninck Y; Trang T
[Ad] Endereço:Department of Comparative Biology and Experimental Medicine, University of Calgary, Calgary, Alberta, Canada.
[Ti] Título:Blocking microglial pannexin-1 channels alleviates morphine withdrawal in rodents.
[So] Source:Nat Med;23(3):355-360, 2017 Mar.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Opiates are essential for treating pain, but termination of opiate therapy can cause a debilitating withdrawal syndrome in chronic users. To alleviate or avoid the aversive symptoms of withdrawal, many of these individuals continue to use opiates. Withdrawal is therefore a key determinant of opiate use in dependent individuals, yet its underlying mechanisms are poorly understood and effective therapies are lacking. Here, we identify the pannexin-1 (Panx1) channel as a therapeutic target in opiate withdrawal. We show that withdrawal from morphine induces long-term synaptic facilitation in lamina I and II neurons within the rodent spinal dorsal horn, a principal site of action for opiate analgesia. Genetic ablation of Panx1 in microglia abolished the spinal synaptic facilitation and ameliorated the sequelae of morphine withdrawal. Panx1 is unique in its permeability to molecules up to 1 kDa in size and its release of ATP. We show that Panx1 activation drives ATP release from microglia during morphine withdrawal and that degrading endogenous spinal ATP by administering apyrase produces a reduction in withdrawal behaviors. Conversely, we found that pharmacological inhibition of ATP breakdown exacerbates withdrawal. Treatment with a Panx1-blocking peptide ( panx) or the clinically used broad-spectrum Panx1 blockers, mefloquine or probenecid, suppressed ATP release and reduced withdrawal severity. Our results demonstrate that Panx1-mediated ATP release from microglia is required for morphine withdrawal in rodents and that blocking Panx1 alleviates the severity of withdrawal without affecting opiate analgesia.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Conexinas/genética
Microglia/efeitos dos fármacos
Morfina/efeitos adversos
Entorpecentes/efeitos adversos
Proteínas do Tecido Nervoso/genética
Células do Corno Posterior/efeitos dos fármacos
Síndrome de Abstinência a Substâncias/genética
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Apirase/farmacologia
Western Blotting
Técnicas de Cultura de Células
Técnicas de Cocultura
Conexinas/antagonistas & inibidores
Conexinas/metabolismo
Mefloquina/farmacologia
Camundongos
Microglia/metabolismo
Naloxona/farmacologia
Antagonistas de Entorpecentes/efeitos adversos
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Nociceptividade/efeitos dos fármacos
Células do Corno Posterior/metabolismo
Probenecid/farmacologia
Ratos
Síndrome de Abstinência a Substâncias/etiologia
Síndrome de Abstinência a Substâncias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (Narcotic Antagonists); 0 (Narcotics); 0 (Nerve Tissue Proteins); 0 (Panx1 protein, mouse); 0 (pannexin 1, rat); 36B82AMQ7N (Naloxone); 76I7G6D29C (Morphine); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.5 (Apyrase); PO572Z7917 (Probenecid); TML814419R (Mefloquine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4281


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[PMID]:28040245
[Au] Autor:Rai SK; Aviña-Zubieta JA; McCormick N; De Vera MA; Shojania K; Sayre EC; Choi HK
[Ad] Endereço:Arthritis Research Canada, Vancouver, British Columbia, Canada; Department of Experimental Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:The rising prevalence and incidence of gout in British Columbia, Canada: Population-based trends from 2000 to 2012.
[So] Source:Semin Arthritis Rheum;46(4):451-456, 2017 Feb.
[Is] ISSN:1532-866X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Gout is increasingly recognized as the most common form of inflammatory arthritis worldwide; however, no Canadian data on the disease burden of gout are available. We estimated the prevalence, incidence, prescription patterns, and comorbidity burden of gout in an entire Canadian province [British Columbia (BC)] over the last decade. METHODS: We utilized PopulationData BC, a province-wide database, to estimate temporal trends in the prevalence and incidence of gout from 2000 to 2012, as well as according to age category. Annual estimates were age-sex-standardized using 2012 as the reference. We also examined annual trends in prescription patterns of common gout medications and assessed the comorbidity burden among gout patients in 2012. RESULTS: The 2012 prevalence of gout was 3.8% among the overall population, and the incidence rate was 2.9 per 1000 person-years. Both gout prevalence and incidence increased substantially over the study period. This burden additionally increased according to age category, affecting over 8% of those ages 60-69 years in 2012. Approximately 22% of gout patients received a prescription for urate-lowering therapy (ULT), which remained stable over the study period, while colchicine and oral glucocorticoid use both increased modestly. By 2012, 72%, 52%, and 18% of prevalent gout patients had been diagnosed with hypertension, hyperlipidemia, and diabetes, respectively. CONCLUSIONS: The burden of gout in BC, Canada, is substantial, and both the prevalence and incidence have increased over the past decade, while prescription of ULT remains low. These data support the need to improve gout prevention and care.
[Mh] Termos MeSH primário: Gota/epidemiologia
[Mh] Termos MeSH secundário: Idoso
Alopurinol/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Colúmbia Britânica/epidemiologia
Colchicina/uso terapêutico
Comorbidade
Diabetes Mellitus/epidemiologia
Febuxostat/uso terapêutico
Feminino
Glucocorticoides/uso terapêutico
Gota/tratamento farmacológico
Supressores da Gota/uso terapêutico
Seres Humanos
Hiperlipidemias/epidemiologia
Hipertensão/epidemiologia
Incidência
Masculino
Meia-Idade
Crescimento Demográfico
Prevalência
Probenecid/uso terapêutico
Sulfimpirazona/uso terapêutico
Uricosúricos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Glucocorticoids); 0 (Gout Suppressants); 0 (Uricosuric Agents); 101V0R1N2E (Febuxostat); 63CZ7GJN5I (Allopurinol); PO572Z7917 (Probenecid); SML2Y3J35T (Colchicine); V6OFU47K3W (Sulfinpyrazone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170102
[St] Status:MEDLINE



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