Base de dados : MEDLINE
Pesquisa : D12.776.260.615.249 [Categoria DeCS]
Referências encontradas : 345 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 35 ir para página                         

  1 / 345 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460056
[Au] Autor:Hayashi G; Jasoliya M; Sahdeo S; Saccà F; Pane C; Filla A; Marsili A; Puorro G; Lanzillo R; Brescia Morra V; Cortopassi G
[Ad] Endereço:Department of Molecular Biosciences, University of California, Davis, 95616 CA, USA.
[Ti] Título:Dimethyl fumarate mediates Nrf2-dependent mitochondrial biogenesis in mice and humans.
[So] Source:Hum Mol Genet;26(15):2864-2873, 2017 08 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The induction of mitochondrial biogenesis could potentially alleviate mitochondrial and muscle disease. We show here that dimethyl fumarate (DMF) dose-dependently induces mitochondrial biogenesis and function dosed to cells in vitro, and also dosed in vivo to mice and humans. The induction of mitochondrial gene expression is more dependent on DMF's target Nrf2 than hydroxycarboxylic acid receptor 2 (HCAR2). Thus, DMF induces mitochondrial biogenesis primarily through its action on Nrf2, and is the first drug demonstrated to increase mitochondrial biogenesis with in vivo human dosing. This is the first demonstration that mitochondrial biogenesis is deficient in Multiple Sclerosis patients, which could have implications for MS pathophysiology and therapy. The observation that DMF stimulates mitochondrial biogenesis, gene expression and function suggests that it could be considered for mitochondrial disease therapy and/or therapy in muscle disease in which mitochondrial function is important.
[Mh] Termos MeSH primário: Fumarato de Dimetilo/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Fumarato de Dimetilo/química
Fibroblastos
Fator de Transcrição de Proteínas de Ligação GA
Seres Humanos
Camundongos
Mitocôndrias/metabolismo
Esclerose Múltipla/metabolismo
Esclerose Múltipla/patologia
Fator 2 Relacionado a NF-E2/genética
Fármacos Neuroprotetores/farmacologia
Biogênese de Organelas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GA-Binding Protein Transcription Factor); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Neuroprotective Agents); 0 (Nfe2l2 protein, mouse); FO2303MNI2 (Dimethyl Fumarate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180225
[Lr] Data última revisão:
180225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx167


  2 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28334913
[Au] Autor:Moujalled D; Grubman A; Acevedo K; Yang S; Ke YD; Moujalled DM; Duncan C; Caragounis A; Perera ND; Turner BJ; Prudencio M; Petrucelli L; Blair I; Ittner LM; Crouch PJ; Liddell JR; White AR
[Ad] Endereço:Department of Pathology, The University of Melbourne, Victoria 3010, Australia.
[Ti] Título:TDP-43 mutations causing amyotrophic lateral sclerosis are associated with altered expression of RNA-binding protein hnRNP K and affect the Nrf2 antioxidant pathway.
[So] Source:Hum Mol Genet;26(9):1732-1746, 2017 May 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:TAR DNA binding protein 43 (TDP-43) is a major disease-associated protein involved in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U). Our previous studies found a direct association between TDP-43 and heterogeneous nuclear ribonucleoprotein K (hnRNP K). In this study, utilizing ALS patient fibroblasts harboring a TDP-43M337V mutation and NSC-34 motor neuronal cell line expressing TDP-43Q331K mutation, we show that hnRNP K expression is impaired in urea soluble extracts from mutant TDP-43 cell models. This was confirmed in vivo using TDP-43Q331K and inducible TDP-43A315T murine ALS models. We further investigated the potential pathological effects of mutant TDP-43-mediated changes to hnRNP K metabolism by RNA binding immunoprecipitation analysis. hnRNP K protein was bound to antioxidant NFE2L2 transcripts encoding Nrf2 antioxidant transcription factor, with greater enrichment in TDP-43M337V patient fibroblasts compared to healthy controls. Subsequent gene expression profiling revealed an increase in downstream antioxidant transcript expression of Nrf2 signaling in the spinal cord of TDP-43Q331K mice compared to control counterparts, yet the corresponding protein expression was not up-regulated in transgenic mice. Despite the elevated expression of antioxidant transcripts, we observed impaired levels of glutathione (downstream Nrf2 antioxidant) in TDP-43M337V patient fibroblasts and astrocyte cultures from TDP-43Q331K mice, indicative of elevated oxidative stress and failure of some upregulated antioxidant genes to be translated into protein. Our findings indicate that further exploration of the interplay between hnRNP K (or other hnRNPs) and Nrf2-mediated antioxidant signaling is warranted and may be an important driver for motor neuron degeneration in ALS.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Ribonucleoproteínas Nucleares Heterogêneas Grupo K/genética
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/genética
Esclerose Amiotrófica Lateral/metabolismo
Animais
Antioxidantes
Linhagem Celular
Demência Frontotemporal/metabolismo
Degeneração Lobar Frontotemporal/genética
Fator de Transcrição de Proteínas de Ligação GA/genética
Ribonucleoproteínas Nucleares Heterogêneas Grupo K/metabolismo
Ribonucleoproteínas Nucleares Heterogêneas/genética
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios Motores/metabolismo
Mutação
Fator 2 Relacionado a NF-E2/metabolismo
RNA/metabolismo
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (DNA-Binding Proteins); 0 (GA-Binding Protein Transcription Factor); 0 (Heterogeneous-Nuclear Ribonucleoprotein K); 0 (Heterogeneous-Nuclear Ribonucleoproteins); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (TDP-43 protein, human); 63231-63-0 (RNA)
[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:170324
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx093


  3 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28294699
[Au] Autor:Santos-López JA; Garcimartín A; López-Oliva ME; Bautista-Ávila M; González-Muñoz MJ; Bastida S; Benedí J; Sánchez-Muniz FJ
[Ad] Endereço:1 Pharmacology Department, Pharmacy School, Complutense University of Madrid, Madrid, Spain .
[Ti] Título:Chia Oil-Enriched Restructured Pork Effects on Oxidative and Inflammatory Status of Aged Rats Fed High Cholesterol/High Fat Diets.
[So] Source:J Med Food;20(5):526-534, 2017 May.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chia oil has the highest recognized α-linolenic acid (ALA) content. ALA is associated with beneficial changes in plasma lipids and the prevention of cardiovascular diseases. Present article aims to analyze the effect of Chia oil-enriched restructured pork (RP) on aged rats in a nonalcoholic steatohepatitis (NASH) model. Groups of six male Wistar rats (1-year old) were fed the experimental diets: control RP diet (C) noncholesterol high saturated; cholesterol-enriched high-saturated fat/high-cholesterol control RP diet (HC) with added cholesterol and cholic acid; and Chia oil- or Hydroxytyrosol RP cholesterol-enriched high-saturated fat/high cholesterol (CHIA and HxT). Total cholesterol, hepatosomatic index, Nrf2, antioxidant, and inflammation markers were determined. CHIA reduced the hypercholesterolemic effect by lowering levels similar to C; also, ameliorated redox index. CHIA, despite high polyunsaturated fatty acids (PUFA) content, reduced thiobarbituric acid reactive substances (TBARS) and induced the lowest SOD protein synthesis but not a reduction on its activity. Chia oil activated the Nrf2 to arrest the pro-oxidative response to cholesterol and aging. Endothelial nitric oxide synthase (eNOS) system was lower in HxT than in CHIA, suggesting its antiatherogenic activity and related protective effect against high PUFA. Increase in tumor necrosis factor alpha (TNFα) was partially blocked by CHIA. Chia oil has the ability to prevent oxidative damage and modify the inflammatory response, suggesting adequate regulation of the antioxidant system. Results stress the importance of incorporating ALA into the diet.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Colesterol na Dieta/efeitos adversos
Hipercolesterolemia/dietoterapia
Carne/análise
Hepatopatia Gordurosa não Alcoólica/dietoterapia
Óleos Vegetais/metabolismo
Salvia/química
[Mh] Termos MeSH secundário: Envelhecimento/efeitos dos fármacos
Envelhecimento/imunologia
Animais
Colesterol na Dieta/metabolismo
Dieta Hiperlipídica/efeitos adversos
Fator de Transcrição de Proteínas de Ligação GA/genética
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Seres Humanos
Hipercolesterolemia/genética
Hipercolesterolemia/imunologia
Hipercolesterolemia/metabolismo
Masculino
Hepatopatia Gordurosa não Alcoólica/genética
Hepatopatia Gordurosa não Alcoólica/imunologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Estresse Oxidativo
Óleos Vegetais/química
Ratos
Ratos Wistar
Suínos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, Dietary); 0 (GA-Binding Protein Transcription Factor); 0 (Gabpa protein, rat); 0 (Plant Oils); 0 (Tumor Necrosis Factor-alpha)
[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:170316
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2016.0161


  4 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28254634
[Au] Autor:Xu P; Lin W; Liu F; Tartakoff A; Tao T
[Ad] Endereço:State Key Laboratory of Stress Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
[Ti] Título:Competitive regulation of IPO4 transcription by ELK1 and GABP.
[So] Source:Gene;613:30-38, 2017 May 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Nuclear import is a highly selective process that involves the specific recognition of appropriate import signals by suitable receptors. Many nuclear transport pathways are mediated by importin ß superfamily members. Among them, IPO4 is a nuclear import receptor for many cargoes. However, its transcriptional regulation remains largely unknown. In the present study, we identified a core region encompassing nt -118 to +108 that is necessary for its promoter activity. Transcription factors binding to this region were screened, resulting in the identification of two members of the Ets family, Ets-like transcription factor-1 and GA binding protein, which repress or activate its promoter activity, respectively. Within this promoter region, two Ets binding sites were identified and shown to be required for promoter activity. Ets-like transcription factor-1 and GA binding protein compete with each other to regulate its promoter activity via its downstream Ets binding sites, as evidenced by EMSA and a luciferase reporter assay. Overexpression of Ets-like transcription factor-1 or GA binding protein results in its down-regulation or up-regulation in cells. Therefore, both Ets-like transcription factor-1 and GA binding protein regulate IPO4 transcription.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Proteínas de Membrana Transportadoras/genética
Proteínas Elk-1 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Regulação para Baixo
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Células HEK293
Seres Humanos
Regiões Promotoras Genéticas
Transcrição Genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ELK1 protein, human); 0 (GA-Binding Protein Transcription Factor); 0 (Membrane Transport Proteins); 0 (ets-Domain Protein Elk-1); 0 (importin 4, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE


  5 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28108517
[Au] Autor:Zhang T; Xu M; Makowski MM; Lee C; Kovacs M; Fang J; Willems E; Trent JM; Hayward NK; Vermeulen M; Brown KM
[Ad] Endereço:Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, NCI, NIH, Bethesda, Maryland.
[Ti] Título: Promoter Mutations Ablate GABP Transcription Factor Binding in Melanoma.
[So] Source:Cancer Res;77(7):1649-1661, 2017 Apr 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:encodes subunit D of the succinate dehydrogenase complex, an integral membrane protein. Across cancer types, recurrent promoter mutations were reported to occur exclusively in melanomas, at a frequency of 4% to 5%. These mutations are predicted to disrupt consensus ETS transcription factor-binding sites and are correlated with both reduced gene expression and poor prognosis. However, the consequence of these mutations on expression in melanoma is still unclear. Here, we found that expression of in melanoma correlated with the expression of multiple ETS transcription factors, particularly in promoter wild-type samples. Consistent with the predicted loss of ETS transcription factor binding, we observed that recurrent hotspot mutations resulted in decreased luciferase activity in reporter assays. Furthermore, we demonstrated specific GABPA and GABPB1 binding to probes containing the wild-type promoter sequences, with binding disrupted by the hotspot promoter mutations in both quantitative mass spectrometry and band-shift experiments. Finally, using siRNA-mediated knockdown across multiple melanoma cell lines, we determined that loss of GABPA resulted in reduced SDHD expression at both RNA and protein levels. These data are consistent with a key role for GABPA/B1 as the critical ETS transcription factors deregulating expression in the context of highly recurrent promoter mutations in melanoma and warrant a detailed search for other recurrent promoter mutations that create or disrupt GABPA consensus sequences. .
[Mh] Termos MeSH primário: Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Melanoma/genética
Mutação
Regiões Promotoras Genéticas
Succinato Desidrogenase/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
Melanoma/metabolismo
Proteínas Proto-Oncogênicas c-ets/metabolismo
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GA-Binding Protein Transcription Factor); 0 (GABPA protein, human); 0 (GABPB1 protein, human); 0 (Proto-Oncogene Proteins c-ets); 0 (SDHD protein, human); EC 1.3.99.1 (Succinate Dehydrogenase)
[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:170122
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-0919


  6 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27760386
[Au] Autor:Holowiecki A; O'Shields B; Jenny MJ
[Ad] Endereço:Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA.
[Ti] Título:Spatiotemporal expression and transcriptional regulation of heme oxygenase and biliverdin reductase genes in zebrafish (Danio rerio) suggest novel roles during early developmental periods of heightened oxidative stress.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;191:138-151, 2017 Jan.
[Is] ISSN:1532-0456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heme oxygenase 1 (HMOX1) degrades heme into biliverdin, which is subsequently converted to bilirubin by biliverdin reductase (BVRa or BVRb) in a manner analogous to the classic anti-oxidant glutathione-recycling pathway. To gain a better understanding of the potential antioxidant roles the BVR enzymes may play during development, the spatiotemporal expression and transcriptional regulation of zebrafish hmox1a, bvra and bvrb were characterized under basal conditions and in response to pro-oxidant exposure. All three genes displayed spatiotemporal expression patterns consistent with classic hematopoietic progenitors during development. Transient knockdown of Nrf2a did not attenuate the ability to detect bvra or bvrb by ISH, or alter spatial expression patterns in response to cadmium exposure. While hmox1a:mCherry fluorescence was documented within the intermediate cell mass, a transient location of primitive erythrocyte differentiation, expression was not fully attenuated in Nrf2a morphants, but real-time RT-PCR demonstrated a significant reduction in hmox1a expression. Furthermore, Gata-1 knockdown did not attenuate hmox1a:mCherry fluorescence. However, while there was a complete loss of detection of bvrb expression by ISH at 24hpf, bvra expression was greatly attenuated but still detectable in Gata-1 morphants. In contrast, 96 hpf Gata-1 morphants displayed increased bvra and bvrb expression within hematopoietic tissues. Finally, temporal expression patterns of enzymes involved in the generation and maintenance of NADPH were consistent with known changes in the cellular redox state during early zebrafish development. Together, these data suggest that Gata-1 and Nrf2a play differential roles in regulating the heme degradation enzymes during an early developmental period of heightened cellular stress.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Regulação Enzimológica da Expressão Gênica
Heme Oxigenase-1/genética
Estresse Oxidativo
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/genética
Transcrição Genética
Proteínas de Peixe-Zebra/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Sítios de Ligação
Compostos de Cádmio/toxicidade
Fator de Transcrição de Proteínas de Ligação GA/genética
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Fator de Transcrição GATA1/genética
Fator de Transcrição GATA1/metabolismo
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Hematopoese
Heme Oxigenase-1/metabolismo
NADP/metabolismo
Oxirredução
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/metabolismo
Regiões Promotoras Genéticas
Fatores de Tempo
Transcrição Genética/efeitos dos fármacos
Peixe-Zebra/embriologia
Peixe-Zebra/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadmium Compounds); 0 (GA-Binding Protein Transcription Factor); 0 (GATA1 Transcription Factor); 0 (Nrf2a protein, zebrafish); 0 (Zebrafish Proteins); 0 (gata1 protein, zebrafish); 53-59-8 (NADP); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (heme oxygenase 1, zebrafish); EC 1.3.- (Oxidoreductases Acting on CH-CH Group Donors); EC 1.3.1.24 (biliverdin reductase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE


  7 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27026184
[Au] Autor:Bellaver B; Souza DG; Souza DO; Quincozes-Santos A
[Ad] Endereço:Departamento de Bioquímica, Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600 - Anexo, Bairro Santa Cecília, Porto Alegre, Rio Grande do Sul, 90035-003, Brazil.
[Ti] Título:Hippocampal Astrocyte Cultures from Adult and Aged Rats Reproduce Changes in Glial Functionality Observed in the Aging Brain.
[So] Source:Mol Neurobiol;54(4):2969-2985, 2017 05.
[Is] ISSN:1559-1182
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Astrocytes are dynamic cells that maintain brain homeostasis, regulate neurotransmitter systems, and process synaptic information, energy metabolism, antioxidant defenses, and inflammatory response. Aging is a biological process that is closely associated with hippocampal astrocyte dysfunction. In this sense, we demonstrated that hippocampal astrocytes from adult and aged Wistar rats reproduce the glial functionality alterations observed in aging by evaluating several senescence, glutamatergic, oxidative and inflammatory parameters commonly associated with the aging process. Here, we show that the p21 senescence-associated gene and classical astrocyte markers, such as glial fibrillary acidic protein (GFAP), vimentin, and actin, changed their expressions in adult and aged astrocytes. Age-dependent changes were also observed in glutamate transporters (glutamate aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1)) and glutamine synthetase immunolabeling and activity. Additionally, according to in vivo aging, astrocytes from adult and aged rats showed an increase in oxidative/nitrosative stress with mitochondrial dysfunction, an increase in RNA oxidation, NADPH oxidase (NOX) activity, superoxide levels, and inducible nitric oxide synthase (iNOS) expression levels. Changes in antioxidant defenses were also observed. Hippocampal astrocytes also displayed age-dependent inflammatory response with augmentation of proinflammatory cytokine levels, such as TNF-α, IL-1ß, IL-6, IL-18, and messenger RNA (mRNA) levels of cyclo-oxygenase 2 (COX-2). Furthermore, these cells secrete neurotrophic factors, including glia-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), S100 calcium-binding protein B (S100B) protein, and transforming growth factor-ß (TGF-ß), which changed in an age-dependent manner. Classical signaling pathways associated with aging, such as nuclear factor erythroid-derived 2-like 2 (Nrf2), nuclear factor kappa B (NFκB), heme oxygenase-1 (HO-1), and p38 mitogen-activated protein kinase (MAPK), were also changed in adult and aged astrocytes and are probably related to the changes observed in senescence marker, glutamatergic metabolism, mitochondrial dysfunction, oxidative/nitrosative stress, antioxidant defenses, inflammatory response, and trophic factors release. Together, our results reinforce the role of hippocampal astrocytes as a target for understanding the mechanisms involved in aging and provide an innovative tool for studies of astrocyte roles in physiological and pathological aging brain.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Astrócitos/metabolismo
Astrócitos/patologia
Hipocampo/metabolismo
Hipocampo/patologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Comportamento Animal
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Forma Celular
Células Cultivadas
Senescência Celular
Cognição
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Proteínas do Citoesqueleto/metabolismo
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Glutamato-Amônia Ligase/metabolismo
Inflamação/patologia
Masculino
NF-kappa B/metabolismo
Estresse Oxidativo
Ratos Wistar
Proteínas S100/metabolismo
Transdução de Sinais
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Cytoskeletal Proteins); 0 (GA-Binding Protein Transcription Factor); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (NF-kappa B); 0 (S100 Proteins); EC 6.3.1.2 (Glutamate-Ammonia Ligase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE
[do] DOI:10.1007/s12035-016-9880-8


  8 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26796989
[Au] Autor:Shang AJ; Yang Y; Wang HY; Tao BZ; Wang J; Wang ZF; Zhou DB
[Ad] Endereço:a Department of Neurosurgery , General Hospital of Chinese PLA , Beijing , People's Republic of China.
[Ti] Título:Spinal cord injury effectively ameliorated by neuroprotective effects of rosmarinic acid.
[So] Source:Nutr Neurosci;20(3):172-179, 2017 Apr.
[Is] ISSN:1476-8305
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Pathophysiology of spinal cord injury (SCI) causes primary and secondary effects leading to loss of neuronal function. The aim of the present study was to investigate the role of rosmarinic acid (RA) in protection against SCI. METHODS: The experimental study was carried out in male wistar rats categorized into three groups. Group I - sham operated rats; Group II - SCI; Group III - SCI followed by RA treatment (10 mg/kg). The spinal tissues after treatment schedule were analyzed for oxidative stress status through determination of reactive oxygen species (ROS), lipid peroxidation, protein damage (carbonyl and sulfhydryl contents), and antioxidant enzyme activities. The expression of oxidative stress factors NF-κB and Nrf-2 was determined by Western blot analysis. Further pro-inflammatory cytokines (TNF-α, IL-6, MCP-1, and IL-1ß) were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The results show that treatment with RA significantly enhances the antioxidant status and decrease the oxidative stress in wistar rats post-SCI. RA effectively ameliorated inflammatory mechanisms by downregulation of NF-κB and pro-inflammatory cytokines post-SCI. CONCLUSION: The study demonstrates for the first time on the role of RA in protecting the spinal cord from injury and demonstrates its neuroprotection in wistar rats.
[Mh] Termos MeSH primário: Cinamatos/uso terapêutico
Depsídeos/uso terapêutico
Modelos Animais de Doenças
Neurônios Motores/efeitos dos fármacos
Fármacos Neuroprotetores/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
Traumatismos da Medula Espinal/tratamento farmacológico
Medula Espinal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Animais
Anti-Inflamatórios não Esteroides/administração & dosagem
Anti-Inflamatórios não Esteroides/uso terapêutico
Antioxidantes/administração & dosagem
Antioxidantes/uso terapêutico
Apoptose/efeitos dos fármacos
Biomarcadores/metabolismo
Cinamatos/administração & dosagem
Depsídeos/administração & dosagem
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Injeções Intraperitoneais
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Neurônios Motores/imunologia
Neurônios Motores/metabolismo
Neurônios Motores/patologia
NF-kappa B/metabolismo
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/metabolismo
Fármacos Neuroprotetores/administração & dosagem
Carbonilação Proteica/efeitos dos fármacos
Ratos Wistar
Espécies Reativas de Oxigênio/antagonistas & inibidores
Espécies Reativas de Oxigênio/metabolismo
Medula Espinal/imunologia
Medula Espinal/metabolismo
Medula Espinal/patologia
Traumatismos da Medula Espinal/imunologia
Traumatismos da Medula Espinal/metabolismo
Traumatismos da Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antioxidants); 0 (Biomarkers); 0 (Cinnamates); 0 (Depsides); 0 (GA-Binding Protein Transcription Factor); 0 (NF-kappa B); 0 (Nerve Tissue Proteins); 0 (Neuroprotective Agents); 0 (Reactive Oxygen Species); MQE6XG29YI (rosmarinic acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1080/1028415X.2015.1103460


  9 / 345 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27912877
[Au] Autor:Arjinajarn P; Pongchaidecha A; Chueakula N; Jaikumkao K; Chatsudthipong V; Mahatheeranont S; Norkaew O; Chattipakorn N; Lungkaphin A
[Ad] Endereço:Department of Biology, Faculty of Science, Chiang Mai University, Chiang Mai, Thailand.
[Ti] Título:Riceberry bran extract prevents renal dysfunction and impaired renal organic anion transporter 3 (Oat3) function by modulating the PKC/Nrf2 pathway in gentamicin-induced nephrotoxicity in rats.
[So] Source:Phytomedicine;23(14):1753-1763, 2016 Dec 15.
[Is] ISSN:1618-095X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study investigated the protective effects of Riceberry bran extract (RBBE) on renal function, and the function and expression of renal organic anion transporter 3 (Oat3) in gentamicin-induced nephrotoxicity in rats and explored the mechanisms for its protective effects. MATERIAL AND METHODS: Male Sprague Dawley rats (n= 42) were divided into six groups to receive normal saline, gentamicin (100mg/kg), co-treatment of gentamicin and RBBE (at dose of 250, 500 and 1000mg/kg), and RBBE (at dose of 1000mg/kg) only, for consecutive fifteen days. Renal function, oxidative and antioxidative markers, the function and expression of Oat3 and histological changes in the kidney were evaluated. RESULTS: Elevation of BUN, serum creatinine levels and reduction in urine creatinine and creatinine clearance indicated decreased renal function in the gentamicin-treated rats. The decrease of [ H]ES uptake in the renal cortical slices of these rats, reflecting the attenuation of Oat3 transport function that was accompanied by decreased expression of Oat3. Moreover, increased MDA level and reduced superoxide dismutase (SOD) and glutathione (GSH) activities were found in gentamicin-treated rats compared to the control group. These changes were associated with the upregulated PKCα, Nrf-2, Keap 1, NQO-1 and HO-1 expressions in kidneys. RBBE treatment improved the renal function and Oat3 transport function and expression in gentamicin-treated rats. The oxidative status was also restored by RBBE treatment. CONCLUSION: RBBE protects kidney injury by its antioxidant effect, subsequently leading to modulation of the PKC/Nrf2 antioxidant defense pathway.
[Mh] Termos MeSH primário: Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Gentamicinas/efeitos adversos
Rim/efeitos dos fármacos
Transportadores de Ânions Orgânicos/metabolismo
Oryza
Extratos Vegetais/farmacologia
Proteína Quinase C/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Antioxidantes/uso terapêutico
Glutationa/metabolismo
Rim/metabolismo
Rim/fisiopatologia
Nefropatias/tratamento farmacológico
Nefropatias/metabolismo
Testes de Função Renal
Masculino
Fitoterapia
Extratos Vegetais/uso terapêutico
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
Ratos Sprague-Dawley
Sementes
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (GA-Binding Protein Transcription Factor); 0 (Gabpb2 protein, rat); 0 (Gentamicins); 0 (Organic Anion Transporters); 0 (Plant Extracts); 0 (Protective Agents); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.13 (Protein Kinase C); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE


  10 / 345 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27847126
[Au] Autor:Song Y; Huang L; Yu J
[Ad] Endereço:Department of Ophthalmology, The first people's hospital of Nantong, Nantong 226001, China. Electronic address: yu_song05@126.com.
[Ti] Título:Effects of blueberry anthocyanins on retinal oxidative stress and inflammation in diabetes through Nrf2/HO-1 signaling.
[So] Source:J Neuroimmunol;301:1-6, 2016 Dec 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Anthocyanins, which are abundant in blueberries, provide significant protection against many chronic diseases. We investigated the effects of blueberry anthocyanins (BA) on diabetes-induced oxidative stress and inflammation in rat retinas. Male rats were divided randomly into five groups. Intraperitoneal injection of streptozotocin (STZ, 60mg/kg) was used to induce a rat diabetes model. BA at 20, 40, and 80mg/kg were given orally for about 12weeks. The results showed that BA could prevent diabetes-induced weight loss and increased blood glucose. BA also upregulated the antioxidant capacity of the retina, increased the content of glutathione (GSH) and glutathione peroxidase (GPx) activity, and decreased malondialdehyde (MDA) and reactive oxygen species (ROS) levels. Vascular endothelial growth factor (VEGF) and interleukin-1ß (IL-1ß) in the serum of diabetes model rats were upregulated, and BA reversed these changes significantly. Furthermore, BA increased the mRNA levels of Nrf2 and HO-1, as well as the nuclear location of Nrf2 and protein levels of HO-1. These results suggested that BA can protect retinal cells from diabetes-induced oxidative stress and inflammation, and this may be regulated through Nrf2/HO-1 signaling.
[Mh] Termos MeSH primário: Antocianinas/farmacologia
Antocianinas/uso terapêutico
Diabetes Mellitus Experimental/patologia
Inflamação/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Retina/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Mirtilos Azuis (Planta)/química
Peso Corporal/efeitos dos fármacos
Diabetes Mellitus Experimental/complicações
Modelos Animais de Doenças
Fator de Transcrição de Proteínas de Ligação GA/genética
Fator de Transcrição de Proteínas de Ligação GA/metabolismo
Glutationa/metabolismo
Glutationa Peroxidase/metabolismo
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Inflamação/etiologia
Interleucina-1beta/metabolismo
Masculino
Malondialdeído/metabolismo
Ratos
Ratos Sprague-Dawley
Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Blood Glucose); 0 (GA-Binding Protein Transcription Factor); 0 (Gabpa protein, rat); 0 (Interleukin-1beta); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.14.18 (Heme Oxygenase-1); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161117
[St] Status:MEDLINE



página 1 de 35 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde