Base de dados : LILACS
Pesquisa : D03.661.243 [Categoria DeCS]
Referências encontradas : 6 [refinar]
Mostrando: 1 .. 6   no formato [Detalhado]

página 1 de 1

  1 / 6 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-762912
Autor: Zhang, J.; Zheng, L.; Cao, J.; Chen, B.; Jin, D..
Título: Inflammation induced by increased frequency of intermittent hypoxia is attenuated by tempol administration
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;48(12):1115-1121, Dec. 2015. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . 12th Five-Year Plan.
Resumo: The levels of serum inflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) and hypoxia inducible factor-1α (HIF-1α) in heart tissues in response to different frequencies of intermittent hypoxia (IH) and the antioxidant tempol were evaluated. Wistar rats (64 males, 200-220 g) were randomly divided into 6 experimental groups and 2 control groups. Four groups were exposed to IH 10, 20, 30, or 40 times/h. The other 2 experimental groups were challenged with IH (30 times/h) plus tempol, either beginning on day 0 (IH30T0) or on day 29 (IH30T29). After 6 weeks of challenge, serum levels of tumor necrosis factor (TNF)-α, intracellular adhesion molecule (ICAM)-1, and interleukin-10 were measured, and western blot analysis was used to detect NF-κB p65 and HIF-1α in myocardial tissues. Serum levels of TNF-α and ICAM-1 and myocardial expression of NF-κB p65 and HIF-1α were all significantly higher in IH rats than in controls (P<0.001). Increased IH frequency resulted in more significant changes. Administration of tempol in IH rats significantly reduced levels of TNF-α, ICAM-1, NF-κB and HIF-1α compared with the non-tempol-treated group (F=16.936, P<0.001). IH induced an inflammatory response in a frequency-dependent manner. Additionally, HIF-1α and NF-κB were increased following IH administration. Importantly, tempol treatment attenuated this effect.
Descritores: Hipóxia/complicações
Antioxidantes/administração & dosagem
Óxidos N-Cíclicos/administração & dosagem
Inflamação/prevenção & controle
-Hipóxia/sangue
Gasometria
Western Blotting
Ensaio de Imunoadsorção Enzimática
Subunidade alfa do Fator 1 Induzível por Hipóxia/análise
Inflamação/metabolismo
Molécula 1 de Adesão Intercelular/sangue
/sangue
INTERLEUKIN-ABDUCENS NERVE/sangue
Miocárdio/metabolismo
Miocárdio/patologia
NF-kappa B/análise
Ratos Wistar
Marcadores de Spin
Fator de Necrose Tumoral alfa/sangue
Limites: Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  2 / 6 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-699771
Autor: Bassi, E.; Liberman, M.; Martinatti, M.K.; Bortolotto, L.A.; Laurindo, F.R.M..
Título: Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;47(2):119-127, 2/2014. graf.
Idioma: en.
Projeto: FAPESP; . FAPESP; . FAPESP; . FAPESP; . FAPESP.
Resumo: Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (controls) or a 0.5% cholesterol (chol) diet+104 IU/day vitamin D2 (vitD) for 12 weeks, and assigned to treatment with water (vehicle, n=20), 0.12 mmol·kg-1·day-1 LA (n=11) or 0.1 mmol·kg-1·day-1 tempol (n=15). Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.
Descritores: Arteriosclerose/prevenção & controle
Óxidos N-Cíclicos/administração & dosagem
Ácido Tióctico/administração & dosagem
Calcificação Vascular/prevenção & controle
-Aorta Torácica
Arteriosclerose/induzido quimicamente
Arteriosclerose/metabolismo
Complacência (Medida de Distensibilidade)/efeitos dos fármacos
Complacência (Medida de Distensibilidade)/fisiologia
Modelos Animais de Doenças
Marcadores de Spin
Resistência Vascular
Calcificação Vascular/induzido quimicamente
Vasoconstrição/efeitos dos fármacos
Vasoconstrição/fisiologia
Limites: Animais
Masculino
Coelhos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 6 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-622783
Autor: Mendanha, S.A.; Anjos, J.L.V.; Silva, A.H.M.; Alonso, A..
Título: Electron paramagnetic resonance study of lipid and protein membrane components of erythrocytes oxidized with hydrogen peroxide
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;45(6):473-481, June 2012. ilus, tab.
Idioma: en.
Resumo: Electron paramagnetic resonance (EPR) spectroscopy of spin labels was used to monitor membrane dynamic changes in erythrocytes subjected to oxidative stress with hydrogen peroxide (H2O2). The lipid spin label, 5-doxyl stearic acid, responded to dramatic reductions in membrane fluidity, which was correlated with increases in the protein content of the membrane. Membrane rigidity, associated with the binding of hemoglobin (Hb) to the erythrocyte membrane, was also indicated by a spin-labeled maleimide, 5-MSL, covalently bound to the sulfhydryl groups of membrane proteins. At 2% hematocrit, these alterations in membrane occurred at very low concentrations of H2O2 (50 µM) after only 5 min of incubation at 37°C in azide phosphate buffer, pH 7.4. Lipid peroxidation, suggested by oxidative hemolysis and malondialdehyde formation, started at 300 µM H2O2 (for incubation of 3 h), which is a concentration about six times higher than those detected with the probes. Ascorbic acid and α-tocopherol protected the membrane against lipoperoxidation, but did not prevent the binding of proteins to the erythrocyte membrane. Moreover, the antioxidant (+)-catechin, which also failed to prevent the cross-linking of cytoskeletal proteins with Hb, was very effective in protecting erythrocyte ghosts from lipid peroxidation induced by the Fenton reaction. This study also showed that EPR spectroscopy can be useful to assess the molecular dynamics of red blood cell membranes in both the lipid and protein domains and examine oxidation processes in a system that is so vulnerable to oxidation.
Descritores: Antioxidantes/farmacologia
Membrana Eritrocítica/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Peroxidação de Lipídeos/efeitos dos fármacos
Proteínas de Membrana/metabolismo
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
-Ácido Ascórbico/farmacologia
Catequina/farmacologia
Óxidos N-Cíclicos/metabolismo
Espectroscopia de Ressonância de Spin Eletrônica
Membrana Eritrocítica/química
Membrana Eritrocítica/fisiologia
Hemólise
Concentração de Íons de Hidrogênio
Hemoglobinas/metabolismo
Peróxido de Hidrogênio/metabolismo
Fluidez de Membrana/efeitos dos fármacos
Estresse Oxidativo/fisiologia
alfa-Tocoferol/farmacologia
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  4 / 6 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Cabral, A. M
Vasquez, E. C
Texto completo
Id: lil-517800
Autor: Pereira, T. M. C; Balarini, C. M; Silva, I. V; Cabral, A. M; Vasquez, E. C; Meyrelles, S. S.
Título: Endogenous angiotensin II modulates nNOS expression in renovascular hypertension
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(7):685-691, July 2009. graf, tab.
Idioma: en.
Resumo: Nitric oxide (NO) influences renal blood flow mainly as a result of neuronal nitric oxide synthase (nNOS). Nevertheless, it is unclear how nNOS expression is modulated by endogenous angiotensin II, an inhibitor of NO function. We tested the hypothesis that the angiotensin II AT1 receptor and oxidative stress mediated by NADPH oxidase contribute to the modulation of renal nNOS expression in two-kidney, one-clip (2K1C) hypertensive rats. Experiments were performed on male Wistar rats (150 to 170 g body weight) divided into 2K1C (N = 19) and sham-operated (N = 19) groups. nNOS expression in kidneys of 2K1C hypertensive rats (N = 9) was compared by Western blotting to that of 2K1C rats treated with low doses of the AT1 antagonist losartan (10 mg·kg-1·day-1; N = 5) or the superoxide scavenger tempol (0.2 mmol·kg-1·day-1; N = 5), which still remain hypertensive. After 28 days, nNOS expression was significantly increased by 1.7-fold in the clipped kidneys of 2K1C rats and by 3-fold in the non-clipped kidneys of 2K1C rats compared with sham rats, but was normalized by losartan. With tempol treatment, nNOS expression increased 2-fold in the clipped kidneys and 1.4-fold in the non-clipped kidneys compared with sham rats. The changes in nNOS expression were not followed by changes in the enzyme activity, as measured indirectly by the cGMP method. In conclusion, AT1 receptors and oxidative stress seem to be primary stimuli for increased nNOS expression, but this up-regulation does not result in higher enzyme activity.
Descritores: Angiotensina II/fisiologia
Hipertensão Renovascular/enzimologia
NADPH Oxidases/efeitos dos fármacos
Óxido Nítrico Sintase Tipo I/metabolismo
Estresse Oxidativo/efeitos dos fármacos
-Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Angiotensina II/antagonistas & inibidores
Óxidos N-Cíclicos/farmacologia
Modelos Animais de Doenças
Hipertensão Renovascular/fisiopatologia
Losartan/farmacologia
NADPH Oxidases/fisiologia
Estresse Oxidativo/fisiologia
Ratos Wistar
Marcadores de Spin
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  5 / 6 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-502297
Autor: Burguete, Asunción; Estevez, Yannick; Castillo, Denis; González, Germán; Villar, Raquel; Solano, Beatriz; Vicente, Esther; Silanes, Silvia Pérez; Aldana, Ignacio; Monge, Antonio; Sauvain, Michel; Deharo, Eric.
Título: Anti-leishmanial and structure-activity relationship of ring substituted 3-phenyl-1-(1, 4-di-N-oxide quinoxalin-2-yl)-2-propen-1-one derivatives
Fonte: Mem. Inst. Oswaldo Cruz;103(8):778-780, Dec. 2008. tab.
Idioma: en.
Resumo: A series of ring substituted 3-phenyl-1-(1,4-di-N-oxide quinoxalin-2-yl)-2-propen-1-one derivatives were synthesized and tested for in vitro leishmanicidal activity against amastigotes of Leishmania amazonensis in axenical cultures and murine infected macrophages. Structure-activity relationships demonstrated the importance of a radical methoxy at position R3', R4' and R5'. (2E)-3-(3,4,5-trimethoxy-phenyl)-1-(3,6,7-trimethyl-1,4-dioxy-quinoxalin-2-yl)-propenone was the most active. Cytotoxicity on macrophages revealed that this product was almost six times more active than toxic.
Descritores: Antiprotozoários/química
Óxidos N-Cíclicos/química
Leishmania mexicana/efeitos dos fármacos
Quinoxalinas/química
-Antiprotozoários/farmacologia
Antiprotozoários/toxicidade
Óxidos N-Cíclicos/farmacologia
Óxidos N-Cíclicos/toxicidade
Camundongos Endogâmicos BALB C
Macrófagos/efeitos dos fármacos
Testes de Sensibilidade Parasitária
Quinoxalinas/farmacologia
Quinoxalinas/toxicidade
Relação Estrutura-Atividade
Limites: Animais
Feminino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  6 / 6 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Augusto, Ohara
Texto completo
Id: lil-477425
Autor: Augusto, Ohara; Trindade, Daniel F; Linares, Edlaine; Vaz, Sandra M.
Título: Cyclic nitroxides inhibit the toxicity of nitric oxide-derived oxidants: mechanisms and implications
Fonte: An. acad. bras. ciênc;80(1):179-189, Mar. 2008. ilus, graf, tab.
Idioma: en.
Resumo: The substantial therapeutic potential of tempol (4-hydroxy-2,2,6,6-tetramethyl-1-piperidinyloxy) and related cyclic nitroxides as antioxidants has stimulated innumerous studies of their reactions with reactive oxygen species. In comparison, reactions of nitroxides with nitric oxide-derived oxidants have been less frequently investigated. Nevertheless, this is relevant because tempol has also been shown to protect animals from injuries associated with inflammatory conditions, which are characterized by the increased production of nitric oxide and its derived oxidants. Here, we review recent studies addressing the mechanisms by which cyclic nitroxides attenuate the toxicity of nitric oxidederived oxidants. As an example, we present data showing that tempol protects mice from acetaminophen-induced hepatotoxicity and discuss the possible protection mechanism. In view of the summarized studies, it is proposed that nitroxides attenuate tissue injury under inflammatory conditions mainly because of their ability to react rapidly with nitrogen dioxide and carbonate radical. In the process the nitroxides are oxidized to the corresponding oxammonium cation, which, in turn, can be recycled back to the nitroxides by reacting with upstream species, such as peroxynitrite and hydrogen peroxide, or with cellular reductants. An auxiliary protection mechanism may be down-regulation of inducible nitric oxide synthase expression. The possible therapeutic implications of these mechanisms are addressed.

O considerável potencial terapêutico de tempol (4-hidroxi-2,2, 6,6-tetrametil-1piperiniloxila) e nitróxidos cíclicos relacionados como antioxidantes tem estimulado inúmeros estudos de suas reações com espécies reativas derivadas de oxigênio. Em comparação, as reações de nitróxidos com oxidantes derivados do óxido nítrico têm sido investigadas menos frequentemente. Todavia, essas reações são relevantes porque o tempol é também capaz de proteger animais de injúrias associadas a condições inflamatórias, as quais são caracterizadas por uma aumentada produção de óxido nítrico e derivados oxidantes. Aqui, discutimos estudos recentes abordando os mecanismos pelos quais nitróxidos cíclicos atenuam a toxicidade de oxidantes derivados do óxido nítrico. Como um exemplo, apresentamos dados que demonstram que o tempol protege camundongos do dano hepatotóxico promovido por altas doses de acetaminofeno e discutimos o possível mecanismo de proteção. Com base nos estudos sumarizados, é proposto que nitróxidos atenuam a injúria tecidual em condições inflamatórias devido principalmente a sua capacidade de reagir rapidamente com ambos, dióxido de nitrogênio e radical carbonato. Em conseqüência, os nitróxidos são oxidados ao cátion oxamônio correspondente, o qual, por sua vez, pode ser reciclado ao nitróxido através de reações com espécies precursoras, como peroxinitrito e peróxido de hidrogênio, ou com redutores celulares. Um possível mecanismo auxiliar de proteção é a regulação negativa da expressão da sintase do óxido nítrico induzível. As possíveis implicações terapêuticas desses mecanismos são abordadas.
Descritores: Antioxidantes/uso terapêutico
Doença Hepática Induzida por Substâncias e Drogas
Óxidos N-Cíclicos/uso terapêutico
Oxirredução/efeitos dos fármacos
-Acetaminofen/efeitos adversos
Acetaminofen/antagonistas & inibidores
Analgésicos não Entorpecentes/efeitos adversos
Analgésicos não Entorpecentes/antagonistas & inibidores
Antioxidantes/química
Doença Hepática Induzida por Substâncias e Drogas
Óxidos N-Cíclicos/química
Inflamação/metabolismo
Inflamação/prevenção & controle
Óxido Nítrico Sintase/antagonistas & inibidores
Marcadores de Spin
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME



página 1 de 1
   


Refinar a pesquisa
  Base de dados : 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