Base de dados : MEDLINE
Pesquisa : D03.661.243 [Categoria DeCS]
Referências encontradas : 5793 [refinar]
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[PMID]:29231930
[Au] Autor:Jing Y; Cao Q; Hao L; Yang GG; Hu WL; Ji LN; Mao ZW
[Ad] Endereço:MOE Key Laboratory of Bioinorganic and Synthetic Chemistry, School of Chemistry, Sun Yat-Sen University, Guangzhou 510275, China. cesmzw@mail.sysu.edu.cn caoqian3@mail.sysu.edu.cn.
[Ti] Título:A self-assessed photosensitizer: inducing and dual-modal phosphorescence imaging of mitochondria oxidative stress.
[So] Source:Chem Commun (Camb);54(3):271-274, 2018 Jan 02.
[Is] ISSN:1364-548X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Two novel Ir(iii)-nitroxide conjugates have been synthesized as mitochondria-targeted multi-functional theranostic photosensitizers, capable of simultaneously inducing and dual-modal phosphorescence imaging of mitochondrial oxidative stress under two-photon excitation, thus realizing the photodynamic therapy of cancer and self-assessment of their PDT efficacies.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Complexos de Coordenação/farmacologia
Óxidos N-Cíclicos/farmacologia
Irídio/química
Substâncias Luminescentes/farmacologia
Mitocôndrias/metabolismo
Estresse Oxidativo
Fármacos Fotossensibilizantes/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Complexos de Coordenação/química
Óxidos N-Cíclicos/química
Seres Humanos
Peróxido de Hidrogênio/farmacologia
Luz
Substâncias Luminescentes/química
Mitocôndrias/ultraestrutura
Fármacos Fotossensibilizantes/química
Acetato de Tetradecanoilforbol/farmacologia
Nanomedicina Teranóstica
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Coordination Complexes); 0 (Cyclic N-Oxides); 0 (Luminescent Agents); 0 (Photosensitizing Agents); 44448S9773 (Iridium); BBX060AN9V (Hydrogen Peroxide); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[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:171213
[St] Status:MEDLINE
[do] DOI:10.1039/c7cc07797a


  2 / 5793 MEDLINE  
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[PMID]:29283261
[Au] Autor:Xu J; Liu S; Chen G; Chen T; Song T; Wu J; Shi C; He M; Tian J
[Ad] Endereço:State Key Laboratory of Pulp and Paper Engineering, School of Light Industry and Engineering and ‡School of Medicine, South China University of Technology , Guangzhou 510640, P. R. China.
[Ti] Título:Engineering Biocompatible Hydrogels from Bicomponent Natural Nanofibers for Anticancer Drug Delivery.
[So] Source:J Agric Food Chem;66(4):935-942, 2018 Jan 31.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural hydrogels have attracted extensive research interest and shown great potential for many biomedical applications. In this study, a series of biocompatible hydrogels was reported based on the self-assembly of positively charged partially deacetylated α-chitin nanofibers (α-DECHN) and negatively charged 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO)-oxidized cellulose nanofibers (TOCNF) for anticancer drug delivery. The formation mechanisms of the α-DECHN/TOCNF hydrogels with different mixing proportions were studied, and their morphological, mechanical, and swelling properties were comprehensively investigated. Additionally, the drug delivery performance of the hydrogels was compared via sustained release test of an anticancer drug (5-fluorouracil). The results showed that the hydrogel with higher physical cross-linking degree exhibited a higher drug loading efficiency and drug release percentage.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Materiais Biocompatíveis
Quitina/química
Óxidos N-Cíclicos/química
Sistemas de Liberação de Medicamentos
Nanofibras/química
[Mh] Termos MeSH secundário: Celulose/química
Reagentes para Ligações Cruzadas
Preparações de Ação Retardada
Fluoruracila/administração & dosagem
Hidrogéis
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biocompatible Materials); 0 (Cross-Linking Reagents); 0 (Cyclic N-Oxides); 0 (Delayed-Action Preparations); 0 (Hydrogels); 1398-61-4 (Chitin); 9004-34-6 (Cellulose); U3P01618RT (Fluorouracil); VQN7359ICQ (TEMPO)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04210


  3 / 5793 MEDLINE  
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[PMID]:29179205
[Au] Autor:Liu H; Jing X; Dong A; Bai B; Wang H
[Ad] Endereço:Department of Cardiology, Tangdu Hospital, the Fourth Military University, Xi'an, China.
[Ti] Título:Overexpression of TIMP3 Protects Against Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Apoptosis Through ROS/Mapks Pathway.
[So] Source:Cell Physiol Biochem;44(3):1011-1023, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Myocardial ischemia/reperfusion (I/R) injury remains a great challenge in clinical therapy. Tissue inhibitor of metalloproteinases 3 (TIMP3) plays a crucial role in heart physiological and pathophysiological processes. However, the effects of TIMP3 on I/R injury remain unknown. METHODS: C57BL/6 mice were infected with TIMP3 adenovirus by local delivery in myocardium followed by I/R operation or doxorubicin treatment. Neonatal rat cardiomyocytes were pretreated with TIMP3 adenovirus prior to anoxia/reoxygenation (A/R) treatment in vitro. Histology, echocardiography, in vivo phenotypical analysis, flow cytometry and western blotting were used to investigate the altered cardiac function and underlying mechanisms. RESULTS: The results showed that upregulation of TIMP3 in myocardium markedly inhibited myocardial infarct areas and the cardiac dysfunction induced by I/R or by doxorubicin treatment. TUNEL staining revealed that TIMP3 overexpression attenuated I/R-induced myocardial apoptosis, accompanied by decreased Bax/Bcl-2 ratio, Cleaved Caspase-3 and Cleaved Caspase-9 expression. In vitro, A/R-induced cardiomyocyte apoptosis was abrogated by pharmacological inhibition of reactive oxygen species (ROS) production or MAPKs signaling. Attenuation of ROS production reversed A/R-induced MAPKs activation, whereas MAPKs inhibitors showed on effect on ROS production. Furthermore, in vivo or in vitro overexpression of TIMP3 significantly inhibited I/R- or A/R-induced ROS production and MAPKs activation. CONCLUSION: Our findings demonstrate that TIMP3 upregulation protects against cardiac I/R injury through inhibiting myocardial apoptosis. The mechanism may be related to inhibition of ROS-initiated MAPKs pathway. This study suggests that TIMP3 may be a potential therapeutic target for the treatment of I/R injury.
[Mh] Termos MeSH primário: Miocárdio/metabolismo
Inibidor Tecidual de Metaloproteinase-3/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Antracenos/farmacologia
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Caspase 9/metabolismo
Células Cultivadas
Óxidos N-Cíclicos/farmacologia
Doxorrubicina/toxicidade
Ecocardiografia
Coração/diagnóstico por imagem
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Traumatismo por Reperfusão Miocárdica/induzido quimicamente
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Marcadores de Spin
Inibidor Tecidual de Metaloproteinase-3/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Cyclic N-Oxides); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (Spin Labels); 0 (Tissue Inhibitor of Metalloproteinase-3); 0 (bcl-2-Associated X Protein); 1TW30Y2766 (pyrazolanthrone); 80168379AG (Doxorubicin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9); U78ZX2F65X (tempol); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485401


  4 / 5793 MEDLINE  
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[PMID]:29183754
[Au] Autor:Santos GB; Ribeiro ACG; Lima SNP; Trostchansky A; Cerdeira CD; Brigagão MRPL
[Ad] Endereço:Departamento de Bioquímica, Instituto de Ciências Biomédicas, Universidade Federal de Alfenas, Alfenas, MG, Brazil.
[Ti] Título:Nitroxide Tempol down-regulates kinase activities associated with NADPH oxidase function in phagocytic cells and potentially decreases their fungicidal response.
[So] Source:Chem Biol Interact;279:203-209, 2018 Jan 05.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:AIMS: The identification of novel targets to control inflammation in humans is probably the primary challenge that impairs the development of new anti-inflammatory drugs. Therefore, the modulation of intracellular signaling pathways in phagocytes may be an interesting means of achieving this goal. However, this change to signaling can compromise the host's susceptibility to invading pathogens. We investigated whether the antioxidant nitroxide Tempol regulates the activity of kinases associated with the production of oxidants in neutrophils, which affects the fungicidal capability of these cells. MAIN METHODS: The effects of Tempol on PMA- or fMLP-activated neutrophils were examined by oxygen consumption as an index of the oxidative burst, a release of extracellular and total Reactive Oxygen Species (ROS) by chemiluminescence, kinase activities through analysis of ATP consumption during enzyme activities and the dot blot immunoassay and, finally, by neutrophil capacity of killing Candida albicans. KEY FINDINGS: Tempol significantly inhibited the neutrophil oxidative burst in a concentration-dependent manner and decreased oxygen consumption (IC50 = 45 µM) and extracellular/total ROS formation with an increase on the lag period response. In addition, Tempol inhibited neutrophil kinase activities (i.e., a decrease in protein phosphorylation) elicited through different biochemical pathways and consequently impaired the fungicidal activity of these cells. SIGNIFICANCE: Although Tempol has potential anti-inflammatory activity that acts on different intracellular pathways (such as those involving kinases), researchers should be cautious, since this nitroxide down-regulated oxidants production and the fungicidal response of neutrophils.
[Mh] Termos MeSH primário: Candida albicans/fisiologia
Óxidos N-Cíclicos/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
NADPH Oxidases/metabolismo
Fagócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Óxidos N-Cíclicos/química
Regulação para Baixo/efeitos dos fármacos
Inflamação
Masculino
Camundongos
Estrutura Molecular
Neutrófilos/enzimologia
Consumo de Oxigênio
Fosfotransferases/genética
Fosfotransferases/metabolismo
Marcadores de Spin
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Spin Labels); EC 1.6.3.- (NADPH Oxidases); EC 2.7.- (Phosphotransferases); U78ZX2F65X (tempol)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


  5 / 5793 MEDLINE  
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[PMID]:29183043
[Au] Autor:Kamiya T; Nagaoka T; Omae T; Ono S; Otani S; Yoshida A
[Ad] Endereço:Department of Ophthalmology, Asahikawa Medical University, Asahikawa, Japan.
[Ti] Título:Benzo(e)pyrene Inhibits Endothelium-Dependent NO-Mediated Dilation of Retinal Arterioles via Superoxide Production and Endoplasmic Reticulum Stress.
[So] Source:Invest Ophthalmol Vis Sci;58(13):5978-5984, 2017 Nov 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To investigate whether benzo(e)pyrene (B(e)P), a toxicant in cigarette smoke, affects the endothelium-dependent nitric oxide (NO)-induced vasodilation of the retinal arterioles, and whether oxidative stress, distinct protein kinase signaling pathways, and endoplasmic reticulum (ER) stress are associated with the B(e)P-induced effect on the retinal arterioles. Methods: In this in vitro study, porcine retinal arterioles were isolated, cannulated, and pressurized without flow. These vessels were treated with intraluminal administration of B(e)P or B(e)P plus blockers for 180 minutes. Diametric changes to agonists were recorded by videomicroscopy. Results: Intraluminal treatment with 100 µM B(e)P for 180 minutes significantly reduced the arteriolar vasodilation caused by the endothelium-dependent NO-mediated agonists bradykinin and A23187 but not that caused by endothelium-independent NO donor sodium nitroprusside. The adverse effects of B(e)P on the vasodilatory action of bradykinin were prevented by the superoxide scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), the nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase) inhibitor apocynin, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, the p38 mitogen-activated protein kinase inhibitor SB203580, genistein, resveratrol (RSV), and the ER stress inhibitor 4-phenylbutyrate (4-PBA). The xanthine oxidase inhibitor allopurinol did not alter the effect of B(e)P on the vasodilatory action induced by bradykinin. Conclusions: B(e)P decreases the endothelium-dependent NO-induced vasodilation in the retinal arterioles through the production of superoxide from NADPH oxidase, which is linked to JNK and p38 kinase. The results suggested that ER stress is instrumental in B(e)P-induced endothelial dysfunction and that genistein and RSV might preserve endothelial function.
[Mh] Termos MeSH primário: Arteríolas/efeitos dos fármacos
Benzopirenos/farmacologia
Estresse do Retículo Endoplasmático/fisiologia
Vasos Retinianos/efeitos dos fármacos
Superóxidos/metabolismo
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Bradicinina/farmacologia
Óxidos N-Cíclicos/farmacologia
Modelos Animais de Doenças
Marcadores de Spin
Suínos
Vasodilatadores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzopyrenes); 0 (Cyclic N-Oxides); 0 (Spin Labels); 0 (Vasodilator Agents); 11062-77-4 (Superoxides); 63APT6398R (benzo(e)pyrene); S8TIM42R2W (Bradykinin); U78ZX2F65X (tempol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21925


  6 / 5793 MEDLINE  
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[PMID]:28714295
[Au] Autor:Chang Z; Henkensmeier D; Chen R
[Ad] Endereço:Transfercenter Sustainable Electrochemistry, Saarland University, 66125, Saarbrücken, Germany.
[Ti] Título:One-Step Cationic Grafting of 4-Hydroxy-TEMPO and its Application in a Hybrid Redox Flow Battery with a Crosslinked PBI Membrane.
[So] Source:ChemSusChem;10(16):3193-3197, 2017 Aug 24.
[Is] ISSN:1864-564X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:By using a one-step epoxide ring-opening reaction between 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (4-hydroxy-TEMPO) and glycidyltrimethylammonium cation (GTMA ), we synthesized a cation-grafted TEMPO (g -TEMPO) and studied its electrochemical performance against a Zn /Zn anode in a hybrid redox flow battery. To conduct Cl counter anions, a crosslinked methylated polybenzimidazole (PBI) membrane was prepared and placed between the catholyte and anolyte. Compared to 4-hydroxy-TEMPO, the positively charged g - TEMPO exhibits enhanced reaction kinetics. Moreover, flow battery tests with g -TEMPO show improved Coulombic, voltage, and energy efficiencies and cycling stability over 140 cycles. Crossover of active species through the membrane was not detected.
[Mh] Termos MeSH primário: Benzimidazóis/química
Óxidos N-Cíclicos/química
Fontes de Energia Elétrica
Hidroxilamina/química
Membranas Artificiais
Polímeros/química
[Mh] Termos MeSH secundário: Eletroquímica
Metilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Cyclic N-Oxides); 0 (Membranes, Artificial); 0 (Polymers); 0 (poly(benzimidazole)); 2FP81O2L9Z (Hydroxylamine); V55XB6IT82 (TEMPOL-H)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1002/cssc.201701060


  7 / 5793 MEDLINE  
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[PMID]:28689421
[Au] Autor:Li X
[Ad] Endereço:School of Chinese Herbal Medicine and Innovative Research and Development Laboratory of TCM, Guangzhou University of Chinese Medicine , 232 Waihuan East Road, Guangzhou Higher Education Mega Center, Panyu District, Guangzhou, Guangdong 510006, People's Republic of China.
[Ti] Título:2-Phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-Oxide (PTIO ) Radical Scavenging: A New and Simple Antioxidant Assay In Vitro.
[So] Source:J Agric Food Chem;65(30):6288-6297, 2017 Aug 02.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Current in vitro antioxidant assays have several limitations, which frequently cause inconsistent results. The study develops a new antioxidant assay using the 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide radical (PTIO ). After the investigation of various factors, the experimental protocol was briefly recommended as follows: PTIO and the sample solution were added to phosphate buffer (pH 7.4, 50 mM), incubated at 37 °C for 2 h, and then spectrophotometrically measured at 557 nm. The validation test based on 20 pure compounds and 30 lyophilized aqueous extracts suggested that PTIO scavenging had a good linear relationship, stability, and reproducibility. In the ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry analysis, PTIO was observed to give m/z 234 when encountering l-ascorbic acid. As an antioxidant assay, PTIO scavenging possesses four advantages, i.e., oxygen-centered radical, physiological aqueous solution, simple and direct measurement, and less interference from the tested sample. It can also satisfactorily analyze the antioxidant structure-activity relationship. PTIO scavenging has no stereospecificity and is at least involved in H transfer.
[Mh] Termos MeSH primário: Técnicas de Química Analítica/métodos
Óxidos N-Cíclicos/química
Depuradores de Radicais Livres/química
Imidazóis/química
[Mh] Termos MeSH secundário: Ácido Ascórbico/química
Espectrometria de Massas
Espectrofotometria
Relação Estrutura-Atividade
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Free Radical Scavengers); 0 (Imidazoles); 18390-00-6 (2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b02247


  8 / 5793 MEDLINE  
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[PMID]:28688768
[Au] Autor:Chami B; Jeong G; Varda A; Maw AM; Kim HB; Fong GM; Simone M; Rayner BS; Wang XS; Dennis JM; Witting PK
[Ad] Endereço:Discipline of Pathology, Charles Perkins Centre, Sydney Medical School, The University of Sydney, NSW 2006, Australia.
[Ti] Título:The nitroxide 4-methoxy TEMPO inhibits neutrophil-stimulated kinase activation in H9c2 cardiomyocytes.
[So] Source:Arch Biochem Biophys;629:19-35, 2017 Sep 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:After acute myocardial infarction (AMI), neutrophils are recruited to the affected myocardium. Hypochlorous acid (HOCl) produced by neutrophil myeloperoxidase (MPO) damages cardiomyocytes and potentially expands the primary infarct. Rat cardiomyocyte-like cells were incubated with isolated human neutrophils treated with chemical activators in the absence or presence of nitroxide 4-methoxy-Tempo (MetT; 25 µM) for 4, 6 or 24 h; studies with reagent HOCl served as positive control. Treating cardiomyocytes with activated neutrophils or reagent HOCl resulted in a marked increase in protein tyrosine chlorination and a decline in protein tyrosine phosphatase (PTP) activity. On balance our data also supported an increase in phosphorylation of MAPK p38 and ERK1/2 suggestive of an intracellular hyperphosphorylation status and this was accompanied by decreases in cell viability, as judged by assessing caspases-3/7 activity. For cells exposed to activated neutrophils receptor-mediated uptake of transferrin decreased although total matrix metalloproteinase (MMP) activity was unaffected. Addition of MetT ameliorated protein tyrosine chlorination, decreased MAPK activity and restored receptor-mediated transferrin uptake and PTP activity in cardiomyocytes. Overall, adverse effects of neutrophil-derived HOCl on cultured cardiomyocytes were ameliorated by MetT suggesting that nitroxides may be beneficial to inflammatory pathologies, where neutrophil recruitment/activation is a prominent and early feature.
[Mh] Termos MeSH primário: Óxidos N-Cíclicos/farmacologia
Neutrófilos/metabolismo
Proteínas Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Neutrófilos/enzimologia
Especificidade de Órgãos
Estresse Oxidativo/efeitos dos fármacos
Peroxidase/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
Fosforilação/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Ratos
Transferrina/metabolismo
Tirosina/metabolismo
Miosinas Ventriculares/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Transferrin); 42HK56048U (Tyrosine); 95407-69-5 (4-methoxy-2,2,6,6-tetramethylpiperidinyl-1-oxy); EC 1.11.1.7 (Peroxidase); EC 2.7.- (Protein Kinases); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.6.1.- (Ventricular Myosins); VQN7359ICQ (TEMPO)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE


  9 / 5793 MEDLINE  
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[PMID]:28666030
[Au] Autor:Jernigan NL; Naik JS; Weise-Cross L; Detweiler ND; Herbert LM; Yellowhair TR; Resta TC
[Ad] Endereço:Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, United States of America.
[Ti] Título:Contribution of reactive oxygen species to the pathogenesis of pulmonary arterial hypertension.
[So] Source:PLoS One;12(6):e0180455, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary arterial hypertension is associated with a decreased antioxidant capacity. However, neither the contribution of reactive oxygen species to pulmonary vasoconstrictor sensitivity, nor the therapeutic efficacy of antioxidant strategies in this setting are known. We hypothesized that reactive oxygen species play a central role in mediating both vasoconstrictor and arterial remodeling components of severe pulmonary arterial hypertension. We examined the effect of the chemical antioxidant, TEMPOL, on right ventricular systolic pressure, vascular remodeling, and enhanced vasoconstrictor reactivity in both chronic hypoxia and hypoxia/SU5416 rat models of pulmonary hypertension. SU5416 is a vascular endothelial growth factor receptor antagonist and the combination of chronic hypoxia/SU5416 produces a model of severe pulmonary arterial hypertension with vascular plexiform lesions/fibrosis that is not present with chronic hypoxia alone. The major findings from this study are: 1) compared to hypoxia alone, hypoxia/SU5416 exposure caused more severe pulmonary hypertension, right ventricular hypertrophy, adventitial lesion formation, and greater vasoconstrictor sensitivity through a superoxide and Rho kinase-dependent Ca2+ sensitization mechanism. 2) Chronic hypoxia increased medial muscularization and superoxide levels, however there was no effect of SU5416 to augment these responses. 3) Treatment with TEMPOL decreased right ventricular systolic pressure in both hypoxia and hypoxia/SU5416 groups. 4) This effect of TEMPOL was associated with normalization of vasoconstrictor responses, but not arterial remodeling. Rather, medial hypertrophy and adventitial fibrotic lesion formation were more pronounced following chronic TEMPOL treatment in hypoxia/SU5416 rats. Our findings support a major role for reactive oxygen species in mediating enhanced vasoconstrictor reactivity and pulmonary hypertension in both chronic hypoxia and hypoxia/SU5416 rat models, despite a paradoxical effect of antioxidant therapy to exacerbate arterial remodeling in animals with severe pulmonary arterial hypertension in the hypoxia/SU5416 model.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Hipertensão Pulmonar/metabolismo
Artéria Pulmonar/patologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Células Cultivadas
Óxidos N-Cíclicos/administração & dosagem
Endotelina-1/metabolismo
Hipertensão Pulmonar/prevenção & controle
Hipertrofia Ventricular Direita/patologia
Masculino
Artéria Pulmonar/metabolismo
Artéria Pulmonar/fisiopatologia
Ratos
Ratos Sprague-Dawley
Marcadores de Spin
Superóxidos/metabolismo
Vasoconstrição
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Endothelin-1); 0 (Reactive Oxygen Species); 0 (Spin Labels); 11062-77-4 (Superoxides); SY7Q814VUP (Calcium); U78ZX2F65X (tempol)
[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:170701
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180455


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[PMID]:28557296
[Au] Autor:Zhou B; Hu X; Zeng G; Li S; Wen Z; Chen L
[Ad] Endereço:Tianjin Key Laboratory of Molecular Optoelectronic Science, School of Science, Collaborative Innovation Center of Chemical Science and Engineering, Tianjin University, No.92 Weijin Road, Nankai District, Tianjin, 300072, China.
[Ti] Título:Bottom-Up Construction of Porous Organic Frameworks with Built-In TEMPO as a Cathode for Lithium-Sulfur Batteries.
[So] Source:ChemSusChem;10(14):2955-2961, 2017 Jul 21.
[Is] ISSN:1864-564X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Two redox-active porous organic frameworks (POFs) with a built-in radical moiety (TEMPO) and hierarchical porous structures were synthesized through a facile bottom-up strategy and studied as cathode materials for lithium-sulfur (Li-S) batteries. The sulfur loading in these two POFs reached 61 %, benefitting from their large pore volumes. Owing to the highly dense docking sites of TEMPO, sulfur could be covalently immobilized within the porous networks and efficiently inhibit the shuttle effect, thereby significantly improving the cycling performance. The composites TPE-TEMPO-POF-S (TPE=tetraphenylethene) deliver a capacity in excess of 470 mAh g after 200 cycles with a coulombic efficiency of around 100 % at a current rate of 0.1 C. Furthermore, TEMPO-POFs with sulfur embedded showed excellent rate capability with limited capacity loss at rates of 0.1-1 C.
[Mh] Termos MeSH primário: Óxidos N-Cíclicos/química
Fontes de Energia Elétrica
Lítio/química
Compostos Organometálicos/química
Enxofre/química
[Mh] Termos MeSH secundário: Eletroquímica
Eletrodos
Modelos Moleculares
Conformação Molecular
Porosidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Organometallic Compounds); 70FD1KFU70 (Sulfur); 9FN79X2M3F (Lithium); VQN7359ICQ (TEMPO)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1002/cssc.201700749



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