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[PMID]:29409869
[Au] Autor:Tateiwa H; Kawano T; Nishigaki A; Yamanaka D; Aoyama B; Shigematsu-Locatelli M; Eguchi S; Locatelli FM; Yokoyama M
[Ad] Endereço:Department of Anesthesiology and Intensive Care Medicine, Kochi Medical School, Nankoku, Kochi, Japan.
[Ti] Título:The role of hippocampal brain-derived neurotrophic factor in age-related differences in neuropathic pain behavior in rats.
[So] Source:Life Sci;197:56-66, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: This study was aimed to explore the contribution of central brain-derived neurotrophic factor (BDNF) in the neuropathic pain pathogenesis using an aged rodent model. MAIN METHODS: Adult and aged rats were randomly assigned to either a sciatic nerve ligation (SNL) group or a control skin sham surgery group. Sensory behavioral testing were performed on the day before surgery and on the 3rd, 7th, 14th, and 21st days after surgery, followed by measurement of BDNF protein levels in different brain regions. In another experiment, the hippocampal BDNF gene expression after SNL surgery was assessed at different time-points. Furthermore, the analgesic effects of intranasal BDNF administration were tested in SNL animals. KEY FINDINGS: Our behavioral results demonstrated that the hyperalgesia-like behavior after painful nerve injury has a higher incidence in aged rats compared with in adult animals. In particular, the hippocampal BDNF levels were inversely correlated with the probability of hyperalgesia-type behavior, in both brain-region specific and age-dependent manner. Time-course analysis showed that the hippocampal levels of BDNF mRNA in aged and adult rats started to decrease 7 and 14 days after surgery, respectively. However, the decrease was more pronounced in aged animals. Moreover, the repeated intranasal BDNF treatment could restore the central BDNF signaling, counteracting the age-related exacerbation of hyperalgesic behavior. SIGNIFICANCE: Our findings imply that hippocampal BDNF may be related with the pathogenesis of elderly neuropathic pain. Pharmacological data further suggest that brain BDNF may be modifiable in aged neuropathic animals, and therefore, represent a promising target for intervention.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Comportamento Animal
Fator Neurotrófico Derivado do Encéfalo/biossíntese
Regulação da Expressão Gênica
Hipocampo/metabolismo
Neuralgia/metabolismo
[Mh] Termos MeSH secundário: Envelhecimento/patologia
Animais
Hipocampo/patologia
Masculino
Neuralgia/patologia
RNA Mensageiro/biossíntese
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (RNA, Messenger)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


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[PMID]:29341893
[Au] Autor:Khan H; Amin S; Patel S
[Ad] Endereço:Department of Pharmacy, Abdul Wali Khan University, Mardan 23200, Pakistan. Electronic address: hkdr2006@gmail.com.
[Ti] Título:Targeting BDNF modulation by plant glycosides as a novel therapeutic strategy in the treatment of depression.
[So] Source:Life Sci;196:18-27, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Current therapies in clinical practice face strong criticism regarding their efficacy, and side effects, which forced the neuro-researchers to discover novel agents with different mechanistic insights. Glycosides are naturally-occurring plant secondary metabolites with significant medicinal potential and clinical scope as antidepressant. The aim of this review is to focus on the antidepressant effects of glycosides in preclinical studies, with an emphasis on the possible mechanisms. The literature search revealed that only a few phytoglycosides have been evaluated for their relevance in depression alleviation. Through preclinical tests, it has come forth that the efficacy is mediated by the modulation of brain-derived neurotrophic factor (BDFN) in the hippocampus, that is known for promoting synaptic efficacy, neuronal connectivity and neuroplasticity. Thus, attempting the upregulation of BDNF expression by plant glycosides can be a novel therapeutic strategy for the treatment of depression. The outcome of this review can stimulate neuroscientists to evaluate plant-derived glycosides for the treatment of depression, as these structurally-complex and diverse molecules, might usher in a new paradigm in the treatment of depression, with a better efficacy and tolerability.
[Mh] Termos MeSH primário: Antidepressivos/uso terapêutico
Fator Neurotrófico Derivado do Encéfalo/efeitos dos fármacos
Depressão/tratamento farmacológico
Depressão/metabolismo
Glicosídeos/uso terapêutico
Fitoterapia
Plantas/química
[Mh] Termos MeSH secundário: Animais
Antidepressivos/efeitos adversos
Antidepressivos/farmacologia
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Glicosídeos/efeitos adversos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Brain-Derived Neurotrophic Factor); 0 (Glycosides); 0 (brain-derived neurotrophic factor, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29360450
[Au] Autor:Song Z; Ye Y; Zhang Z; Shen J; Hu Z; Wang Z; Zheng J
[Ad] Endereço:Department of Orthopaedics, Suining Central Hospital, Sichuan, People's Republic of China.
[Ti] Título:Noninvasive, targeted gene therapy for acute spinal cord injury using LIFU-mediated BDNF-loaded cationic nanobubble destruction.
[So] Source:Biochem Biophys Res Commun;496(3):911-920, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Various gene delivery systems have been widely studied for the acute spinal cord injury (SCI) treatment. In the present study, a novel type of brain-derived neurotrophic factor (BDNF)-loaded cationic nanobubbles (CNBs) conjugated with MAP-2 antibody (mAb /BDNF/CNBs) was prepared to provide low-intensity focused ultrasound (LIFU)-targeted gene therapy. In vitro experiments, the ultrasound-targeted tranfection to BDNF overexpressioin in neurons and efficiently inhibition neuronal apoptosis have been demonstrated, and the elaborately designed mAb /BDNF/CNBs can specifically target to the neurons. Furthermore, in a acute SCI rat model, LIFU-mediated mAb /BDNF/CNBs transfection significantly increased BDNF expression, attenuated histological injury, decreased neurons loss, inhibited neuronal apoptosis in injured spinal cords, and increased BBB scores in SCI rats. LIFU-mediated mAb /BDNF/CNBs destruction significantly increase transfection efficiency of BDNF gene both in vitro and in vivo, and has a significant neuroprotective effect on the injured spinal cord. Therefore, the combination of LIFU irradiation and gene therapy through mAb /BDNF/CNBs can be considered as a novel non-invasive and targeted treatment for gene therapy of SCI.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/administração & dosagem
Preparações de Ação Retardada/administração & dosagem
Terapia Genética/métodos
Nanocápsulas/efeitos da radiação
Sonicação/métodos
Traumatismos da Medula Espinal/genética
Traumatismos da Medula Espinal/terapia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Fator Neurotrófico Derivado do Encéfalo/genética
Cátions
Fluorcarbonetos/efeitos da radiação
Marcação de Genes/métodos
Ondas de Choque de Alta Energia
Masculino
Terapia de Alvo Molecular/métodos
Nanocápsulas/química
Nanosferas/química
Nanosferas/efeitos da radiação
Ratos
Ratos Sprague-Dawley
Traumatismos da Medula Espinal/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Cations); 0 (Delayed-Action Preparations); 0 (Fluorocarbons); 0 (Nanocapsules); 0 (brain-derived neurotrophic factor, human); CK0N3WH0SR (perflutren)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


  4 / 12931 MEDLINE  
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[PMID]:29305263
[Au] Autor:Cao D; Cui J; Cao D; Guo C; Min G; Liu M; Li L
[Ad] Endereço:Department of Pathology, Capital Medical University, Beijing 100069, China.
[Ti] Título:S-adenosylmethionine reduces the inhibitory effect of Aß on BDNF expression through decreasing methylation level of BDNF exon â…£ in rats.
[So] Source:Biochem Biophys Res Commun;495(4):2609-2615, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The structure of brain-derived neurotrophic factor (BDNF) gene is complex, which is composed of eight non-coding exons and one coding exon, each of them has its own unique promoter. Multiple BDNF transcripts have distinct functional properties and epigenetic modulation of BDNF gene transcription is implicated in the neurological disorders. In the present study, rat models with amyloid-ß (Aß) intrahippocampal injection and PC12 cells were used to explore the role of DNA methylation in the promoters of BDNF exon â…£ and exon â…¥ in BDNF suppression caused by Aß. We found that Aß inhibited BDNF expression accompanying with hypermethylation in BDNF exon â…£ promoter, meanwhile, S-adenosylmethionine (SAM), primary methyl donor, reversed the low BDNF expression through demethylation in BDNF exon â…£ promoter. No methylation change was observed in BDNF exon â…¥ promoter. The alteration of DNA methylation caused by Aß or SAM was mediated by DNA methyltransferase 3A (DNMT3A). These data suggest that methylation change in BDNF exon â…£ is involved in the regulation of BDNF expression by Aß or SAM, and further support the view of specific epigenetic modifications of a certain BDNF gene transcript.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/metabolismo
Fator Neurotrófico Derivado do Encéfalo/genética
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Éxons/genética
Hipocampo/metabolismo
S-Adenosilmetionina/metabolismo
[Mh] Termos MeSH secundário: Peptídeos beta-Amiloides/genética
Animais
Metilação de DNA/genética
Regulação da Expressão Gênica/genética
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Brain-Derived Neurotrophic Factor); 7LP2MPO46S (S-Adenosylmethionine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  5 / 12931 MEDLINE  
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[PMID]:29205667
[Au] Autor:Wang L; Fu H; Liu B; Liu X; Chen W; Yu X
[Ad] Endereço:Department of Developmental and Behavioral Pediatrics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai 200127, China, Shanghai, 200127, China.
[Ti] Título:The effect of postnatal manganese exposure on the NMDA receptor signaling pathway in rat hippocampus.
[So] Source:J Biochem Mol Toxicol;31(12), 2017 Dec.
[Is] ISSN:1099-0461
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Overexposure to manganese (Mn) is associated with neurological disorders in children. Evidence indicated that N-methyl-d-aspartate (NMDA) receptor signaling pathway was critical for neurobehavioral function. However, whether NMDA receptor signaling pathway contributes to Mn-induced neurotoxicity remains unknown. In this study, newborn Sprague-Dawley rats were randomly assigned to four groups exposed to 0, 10, 20, and 30 mg/kg of Mn by intraperitoneal injection (n = 10/group: five males and five females). After 3 weeks of Mn exposure, messenger RNA (mRNA) and protein expression of NMDA receptor subunits (NR1, NR2A, and NR2B), cAMP-response element binding protein (CREB), and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by real-time quantitative RT-PCR and Western blot. In Mn-exposed rats, decreased mRNA and protein expression of NR1, NR2A, and NR2B, CREB, and BDNF was observed. The results imply that downregulated NMDA receptor signaling pathway may be of vital importance in the neuropathological process of Mn-induced neurotoxicity.
[Mh] Termos MeSH primário: Hipocampo/metabolismo
Manganês/toxicidade
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Fator Neurotrófico Derivado do Encéfalo/genética
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Masculino
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Receptors, N-Methyl-D-Aspartate); 42Z2K6ZL8P (Manganese)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1002/jbt.21969


  6 / 12931 MEDLINE  
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[PMID]:28452409
[Au] Autor:Grunebaum MF; Ellis SP; Keilp JG; Moitra VK; Cooper TB; Marver JE; Burke AK; Milak MS; Sublette ME; Oquendo MA; Mann JJ
[Ad] Endereço:Molecular Imaging and Neuropathology Division, Department of Psychiatry, Columbia University Medical Center (CUMC) and New York State Psychiatric Institute, New York, NY, USA.
[Ti] Título:Ketamine versus midazolam in bipolar depression with suicidal thoughts: A pilot midazolam-controlled randomized clinical trial.
[So] Source:Bipolar Disord;19(3):176-183, 2017 May.
[Is] ISSN:1399-5618
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To evaluate feasibility and effects of a sub-anesthetic infusion dose of ketamine versus midazolam on suicidal ideation in bipolar depression. Neurocognitive, blood and saliva biomarkers were explored. METHODS: Sixteen participants with bipolar depression and a Scale for Suicidal Ideation (SSI) score of ≥4 were randomized to ketamine (0.5 mg/kg) or midazolam (0.02 mg/kg). Current pharmacotherapy was maintained excluding benzodiazepines within 24 hours. The primary clinical outcome was SSI score on day 1 post-infusion. RESULTS: Results supported feasibility. Mean reduction of SSI after ketamine infusion was almost 6 points greater than after midazolam, although this was not statistically significant (estimate=5.84, SE=3.01, t=1.94, P=.074, 95% confidence interval ([CI)]=-0.65 to 12.31). The number needed to treat for response (SSI <4 and at least 50% below baseline) was 2.2, and for remission (SSI=0) was 3.2. The strongest neurocognitive correlation was between memory improvement on the Selective Reminding Test (SRT) and reduction in SSI score on day 1 after ketamine (ρ=-.89, P=.007). Pre- to post-infusion decrease in serum brain derived neurotrophic factor (BDNF) correlated with reduction in SSI from baseline to day 1 after ketamine (n=5, ρ=0.90, P=.037) but not midazolam (P=.087). CONCLUSIONS: The study demonstrated feasibility. Suicidal thoughts were lower after ketamine than after midazolam at a trend level of significance, likely due to the small pilot sample. Memory improvement and BDNF are promising biomarkers. Replication is needed in an adequately powered full-scale trial.
[Mh] Termos MeSH primário: Transtorno Bipolar
Ketamina
Memória/efeitos dos fármacos
Midazolam
Ideação Suicida
[Mh] Termos MeSH secundário: Adulto
Anestésicos Dissociativos/administração & dosagem
Anestésicos Dissociativos/efeitos adversos
Biomarcadores/análise
Transtorno Bipolar/diagnóstico
Transtorno Bipolar/tratamento farmacológico
Transtorno Bipolar/psicologia
Fator Neurotrófico Derivado do Encéfalo/análise
Relação Dose-Resposta a Droga
Método Duplo-Cego
Monitoramento de Medicamentos/métodos
Feminino
Moduladores GABAérgicos/administração & dosagem
Moduladores GABAérgicos/efeitos adversos
Seres Humanos
Ketamina/administração & dosagem
Ketamina/efeitos adversos
Masculino
Midazolam/administração & dosagem
Midazolam/efeitos adversos
Meia-Idade
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anesthetics, Dissociative); 0 (Biomarkers); 0 (Brain-Derived Neurotrophic Factor); 0 (GABA Modulators); 0 (brain-derived neurotrophic factor, human); 690G0D6V8H (Ketamine); R60L0SM5BC (Midazolam)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/bdi.12487


  7 / 12931 MEDLINE  
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[PMID]:29286858
[Au] Autor:Ritchie AI; Singanayagam A; Wiater E; Edwards MR; Montminy M; Johnston SL
[Ad] Endereço:1 National Heart and Lung Institute, Imperial College London, United Kingdom.
[Ti] Título:ß -Agonists Enhance Asthma-Relevant Inflammatory Mediators in Human Airway Epithelial Cells.
[So] Source:Am J Respir Cell Mol Biol;58(1):128-132, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos beta 2/farmacologia
Asma/metabolismo
Brônquios/metabolismo
Células Epiteliais/metabolismo
Mediadores da Inflamação/metabolismo
[Mh] Termos MeSH secundário: Asma/patologia
Fator Neurotrófico Derivado do Encéfalo/biossíntese
Brônquios/patologia
Linhagem Celular
Células Epiteliais/patologia
Seres Humanos
Interleucina-11/biossíntese
Interleucina-6/biossíntese
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); 0 (Brain-Derived Neurotrophic Factor); 0 (IL11 protein, human); 0 (IL6 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-11); 0 (Interleukin-6); 0 (brain-derived neurotrophic factor, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0315LE


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[PMID]:29191031
[Au] Autor:Duman RS
[Ad] Endereço:From the Departments of Psychiatry and Neuroscience, Yale University School of Medicine, New Haven, Conn.
[Ti] Título:BDNF, 5-HT, and Anxiety: Identification of a Critical Periadolescent Developmental Period.
[So] Source:Am J Psychiatry;174(12):1137-1139, 2017 12 01.
[Is] ISSN:1535-7228
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Transtornos de Ansiedade
Fator Neurotrófico Derivado do Encéfalo
[Mh] Termos MeSH secundário: Ansiedade
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1176/appi.ajp.2017.17101084


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[PMID]:28456776
[Au] Autor:Verbickas V; Baranauskiene N; Eimantas N; Kamandulis S; Rutkauskas S; Satkunskiene D; Sadauskas S; Brazaitis M; Skurvydas A
[Ad] Endereço:Institute of Sports Science and Innovation, Lithuanian Sports University, Kaunas, Lithuania. v.verbickas@gmail.com.
[Ti] Título:Effect of sprint cycling and stretch-shortening cycle exercises on the neuromuscular, immune and stress indicators in young men.
[So] Source:J Physiol Pharmacol;68(1):125-132, 2017 02.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Selection of optimal physical load is essential for desired adaptation including health benefits. We hypothesized that neuromuscular, immune and stress indicators will be higher after energy demanding sprint interval exercise (SIE) than to mechanically demanding stretch-shortening cycle exercise (SSE). The main aim of this study was to assess and compare the kinetics of blood brain-derived neurotrophic factor (BDNF), norepinephrine (NE) and cortisol (as stress indicators) and proinflammatory (IL-6) and anti-inflammatory (IL-10) cytokines within 24 hours after metabolically demanding SIE and after muscle damage inducing SSE. Twenty healthy physically active young men randomly assigned to two equal groups to complete 12 bouts of 5 s stationary cycling sprints every 3 min (SIE) or 200 drop-jumps with 30 s interval between each jump (SSE), respectively. Quadriceps muscle maximal voluntary contraction torque and voluntary activation and soreness were measured and blood samples collected before and 2 min, 1 hour, 12 hours and 24 hours after the SIE and SSE. The BDNF, cortisol, IL-6 and NE levels increased more at 2 min after SIE than SSE (P < 0.05); however, the IL-10 level did not differ between SIE and SSE. BDNF and cortisol levels were decreased at 24 h after both SIE and especially after SSE. The higher was the initial BDNF level, the greater was its decrease at 24 h after both type of exercise. Before exercise BDNF level correlated closely with the change in central fatigue (decrease in voluntary activation) after both SIE and SSE. We thus conclude that both metabolically demanding SIE and muscle damage inflicting SSE induced long-lasting decrease in circulating BDNF which may not promote brain health. The level of circulating BDNF, but not cortisol, IL-6, IL-10 or NE, was associated with changes in central motor fatigue.
[Mh] Termos MeSH primário: Ciclismo/fisiologia
Exercício/fisiologia
[Mh] Termos MeSH secundário: Adulto
Fator Neurotrófico Derivado do Encéfalo/sangue
Creatina Quinase/sangue
Seres Humanos
Hidrocortisona/sangue
Interleucina-10/sangue
Interleucina-6/sangue
Masculino
Contração Muscular
Fadiga Muscular/imunologia
Fadiga Muscular/fisiologia
Norepinefrina/sangue
Músculo Quadríceps/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (IL10 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (brain-derived neurotrophic factor, human); 130068-27-8 (Interleukin-10); EC 2.7.3.2 (Creatine Kinase); WI4X0X7BPJ (Hydrocortisone); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  10 / 12931 MEDLINE  
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[PMID]:29191454
[Au] Autor:Kraemer ÂB; Parfitt GM; Acosta DDS; Bruch GE; Cordeiro MF; Marins LF; Ventura-Lima J; Monserrat JM; Barros DM
[Ad] Endereço:Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Rio Grande - FURG, Rio Grande, RS, Brazil.
[Ti] Título:Fullerene (C60) particle size implications in neurotoxicity following infusion into the hippocampi of Wistar rats.
[So] Source:Toxicol Appl Pharmacol;338:197-203, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The buckminsterfullerene (C60) is considered as a relevant candidate for drug and gene delivery to the brain, once it has the ability to cross the blood-brain barrier. However, the biological implications of this nanomaterial are not fully understood, and its safety for intracerebral delivery is still debatable. In this study, we investigated if C60 particle size could alter its biological effects. For this, two aqueous C60 suspensions were used with maximum particle size up to 200nm and 450nm. The suspensions were injected in the hippocampus, the main brain structure involved in memory processing and spatial localization. In order to assess spatial learning, male Wistar rats were tested in Morris water maze, and the hippocampal BDNF protein levels and gene expression were analyzed. Animals treated with C60 up to 450nm demonstrated impaired spatial memory with a significant decrease in BDNF protein levels and gene expression. However, an enhanced antioxidant capacity was observed in both C60 treatments. A decrease in reactive oxygen species levels was observed in the treatments with suspensions containing particles measuring with up to 450nm. Thiobarbituric acid reactive substances, glutamate cysteine ligase, and glutathione levels showed no alterations among the different treatments. In conclusion, different particle sizes of the same nanomaterial can lead to different behavioral outcomes and biochemical parameters in brain tissue.
[Mh] Termos MeSH primário: Fulerenos/toxicidade
Hipocampo/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/análise
Hipocampo/metabolismo
Masculino
Tamanho da Partícula
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Fullerenes); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE



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