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[PMID]:28467721
[Au] Autor:Sareila O; Hagert C; Kelkka T; Linja M; Xu B; Kihlberg J; Holmdahl R
[Ad] Endereço:1 Medicity Research Laboratory, University of Turku , Turku, Finland .
[Ti] Título:Reactive Oxygen Species Regulate Both Priming and Established Arthritis, but with Different Mechanisms.
[So] Source:Antioxid Redox Signal;27(18):1473-1490, 2017 Dec 20.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Neutrophil cytosolic factor 1 (NCF1) is a key regulatory component of the phagocytic NOX2 complex, which produces reactive oxygen species (ROS). Polymorphism of the Ncf1 gene is associated with increased arthritis severity. In this study, we generated targeted Ncf1 knock-in mice with inducible Ncf1 expression and determined the critical time window during which the NOX2-derived ROS protect the mice from arthritis. RESULTS: Targeted Ncf1 knock-in mice lacked NOX2-derived ROS, and in vivo allelic conversion of Ncf1 by the CreER recombinase led to full protein expression and ROS production within 10 days. Mice in which Ncf1 had been activated before immunization with type II collagen (CII) developed only mild clinical symptoms of collagen-induced arthritis (CIA), whereas the ROS-deficient littermates had severe arthritis. The functional Ncf1 restricted the expansion of IL-17A-producing T cells specific for the immunodominant CII peptide. When the Ncf1 gene was activated after the priming phase, Ncf1-dependent protection from autoimmune arthritis was still observed, together with a reduced number of splenic monocytes but it was not associated with alterations in peptide-specific T cell response. The Ncf1-deficient mice expressed pronounced interferon signature, which could be normalized by conditional expression of Ncf1 and was also present in the Ncf1-mutated mouse during arthritis. Innovation and Conclusion: Ncf1 deficiency has been known to predispose to autoimmunity in both humans and rodents. Our in vivo results point to a regulatory role of NOX2-derived ROS not only during priming but also during the effector phase of CIA, most likely via different mechanisms. Antioxid. Redox Signal. 27, 1473-1490.
[Mh] Termos MeSH primário: Artrite Experimental/metabolismo
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/induzido quimicamente
Artrite Experimental/genética
Colágeno Tipo II/efeitos adversos
Modelos Animais de Doenças
Técnicas de Introdução de Genes
Seres Humanos
Interleucina-17/metabolismo
Camundongos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Interleukin-17); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (neutrophil cytosolic factor 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2016.6981


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[PMID]:28922779
[Au] Autor:Hanley CJ; Mellone M; Ford K; Thirdborough SM; Mellows T; Frampton SJ; Smith DM; Harden E; Szyndralewiez C; Bullock M; Noble F; Moutasim KA; King EV; Vijayanand P; Mirnezami AH; Underwood TJ; Ottensmeier CH; Thomas GJ
[Ad] Endereço:Cancer Sciences Unit, University of Southampton Faculty of Medicine, Southampton, UK; Genkyotex SA, Plan-les-Ouates, Switzerland; La Jolla Institute for Allergy and Immunology, La Jolla, CA.
[Ti] Título:Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Cancer-associated fibroblasts (CAFs) are tumor-promoting and correlate with poor survival in many cancers, which has led to their emergence as potential therapeutic targets. However, effective methods to manipulate these cells clinically have yet to be developed. Methods: CAF accumulation and prognostic significance in head and neck cancer (oral, n = 260; oropharyngeal, n = 271), and colorectal cancer (n = 56) was analyzed using immunohistochemistry. Mechanisms regulating fibroblast-to-myofibroblast transdifferentiation were investigated in vitro using RNA interference/pharmacological inhibitors followed by polymerase chain reaction (PCR), immunoblotting, immunofluorescence, and functional assays. RNA sequencing/bioinformatics and immunohistochemistry were used to analyze NAD(P)H Oxidase-4 (NOX4) expression in different human tumors. NOX4's role in CAF-mediated tumor progression was assessed in vitro, using CAFs from multiple tissues in Transwell and organotypic culture assays, and in vivo, using xenograft (n = 9-15 per group) and isograft (n = 6 per group) tumor models. All statistical tests were two-sided. Results: Patients with moderate/high levels of myofibroblastic-CAF had a statistically significant decrease in cancer-specific survival rates in each cancer type analyzed (hazard ratios [HRs] = 1.69-7.25, 95% confidence intervals [CIs] = 1.11 to 31.30, log-rank P ≤ .01). Fibroblast-to-myofibroblast transdifferentiation was dependent on a delayed phase of intracellular reactive oxygen species, generated by NOX4, across different anatomical sites and differentiation stimuli. A statistically significant upregulation of NOX4 expression was found in multiple human cancers (P < .001), strongly correlating with myofibroblastic-CAFs (r = 0.65-0.91, adjusted P < .001). Genetic/pharmacological inhibition of NOX4 was found to revert the myofibroblastic-CAF phenotype ex vivo (54.3% decrease in α-smooth muscle actin [α-SMA], 95% CI = 10.6% to 80.9%, P = .009), prevent myofibroblastic-CAF accumulation in vivo (53.2%-79.0% decrease in α-SMA across different models, P ≤ .02) and slow tumor growth (30.6%-64.0% decrease across different models, P ≤ .04). Conclusions: These data suggest that pharmacological inhibition of NOX4 may have broad applicability for stromal targeting across cancer types.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Fibroblastos Associados a Câncer/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Colorretais/química
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Bucais/química
Miofibroblastos/patologia
NADPH Oxidases/antagonistas & inibidores
Neoplasias Orofaríngeas/química
[Mh] Termos MeSH secundário: Actinas/análise
Adenocarcinoma/química
Adenocarcinoma/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Fibroblastos Associados a Câncer/química
Fibroblastos Associados a Câncer/fisiologia
Carcinoma Pulmonar de Células não Pequenas/química
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Escamosas/química
Carcinoma de Células Escamosas/genética
Contagem de Células
Transdiferenciação Celular/efeitos dos fármacos
Transdiferenciação Celular/genética
Neoplasias Colorretais/patologia
Progressão da Doença
Neoplasias Esofágicas/química
Neoplasias Esofágicas/genética
Feminino
Neoplasias de Cabeça e Pescoço/química
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/genética
Seres Humanos
Neoplasias Pulmonares/química
Neoplasias Pulmonares/genética
Masculino
Camundongos
Meia-Idade
Neoplasias Bucais/patologia
Miofibroblastos/química
NADPH Oxidase 4
NADPH Oxidases/análise
NADPH Oxidases/genética
Transplante de Neoplasias
Neoplasias Orofaríngeas/patologia
Fenótipo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Taxa de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (GKT137831); 0 (Pyrazoles); 0 (Pyridines); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx121


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[PMID]:29309410
[Au] Autor:Li Z; Wang F; Zhao Q; Liu J; Cheng F
[Ad] Endereço:College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.
[Ti] Título:Involvement of NADPH oxidase isoforms in the production of O2- manipulated by ABA in the senescing leaves of early-senescence-leaf (esl) mutant rice (Oryza sativa).
[So] Source:PLoS One;13(1):e0190161, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, the differences in reactive oxygen species (ROS) generation and abscisic acid (ABA) accumulation in senescing leaves were investigated by early-senescence-leaf (esl) mutant and its wild type, to clarify the relationship among ABA levels, ROS generation, and NADPH oxidase (Nox) in senescing leaves of rice (Oryza sativa). The temporal expression levels of OsNox isoforms in senescing leaves and their expression patterns in response to ABA treatment were determined through quantitative real-time reverse transcription PCR (qRT-PCR). Results showed that the flag leaf of the esl mutant generated more O2- concentrations and accumulated higher ABA levels than the wild-type cultivar did in the grain-filling stage. Exogenous ABA treatment induced O2- generation; however, it was depressed by diphenyleneiodonium chloride (DPI) pretreatment in the detached leaf segments. This finding suggested the involvement of NADPH oxidase in ABA-induced O2- generation. The esl mutant exhibited significantly higher expression of OsNox2, OsNox5, OsNox6, and OsNox7 in the initial of grain-filling stage, followed by sharply decrease. The transcriptional levels of OsNox1, OsNox3, and OsFR07 in the flag leaf of the esl mutant were significantly lower than those in the wild-type cultivar. The expression levels of OsNox2, OsNox5, OsNox6, and OsNox7 were significantly enhanced by exogenous ABA treatments. The enhanced expression levels of OsNox2 and OsNox6 were dependent on the duration of ABA treatment. The inducible expression levels of OsNox5 and OsNox7 were dependent on ABA concentrations. By contrast, exogenous ABA treatment severely repressed the transcripts of OsNox1, OsNox3, and OsFR07 in the detached leaf segments. Therefore, OsNox2, OsNox5, OsNox6, and OsNox7 were probably involved in the ABA-induced O2- generation in the initial stage of leaf senescence. Subsequently, other oxidases activated in deteriorating cells were associated with ROS generation and accumulation in the senescing leaves of the esl mutant. Conversely, OsNox1, OsNox3, and OsFR07 were not associated with ABA-induced O2- generation during leaf senescence.
[Mh] Termos MeSH primário: Ácido Abscísico/metabolismo
NADPH Oxidases/metabolismo
Oryza/metabolismo
Oxigênio/metabolismo
Folhas de Planta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
72S9A8J5GW (Abscisic Acid); EC 1.6.3.- (NADPH Oxidases); S88TT14065 (Oxygen)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190161


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[PMID]:28455132
[Au] Autor:Boonprom P; Boonla O; Chayaburakul K; Welbat JU; Pannangpetch P; Kukongviriyapan U; Kukongviriyapan V; Pakdeechote P; Prachaney P
[Ad] Endereço:Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
[Ti] Título:Garcinia mangostana pericarp extract protects against oxidative stress and cardiovascular remodeling via suppression of p47 and iNOS in nitric oxide deficient rats.
[So] Source:Ann Anat;212:27-36, 2017 Jul.
[Is] ISSN:1618-0402
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:N -Nitro-l-arginine methyl ester (l-NAME)-induced hypertension and cardiovascular remodeling are associated with oxidative stress and inflammation. Garcinia mangostana Linn., has been reported to have antioxidant and anti-inflammatory properties. This study investigated whether G. mangostana pericarp extract (GME) could prevent l-NAME-induced hemodynamic alterations, cardiovascular remodeling, oxidative stress and inflammation in rats. Male Sprague-Dawley rats were given 40mg/kg/day of l-NAME in drinking water to induce hypertension, and were simultaneously treated with GME at a dose of 200mg/kg/day. Rats that received l-NAME for five weeks had high blood pressure, left ventricular hypertrophy and thickening of aortic wall. Vascular superoxide production, plasma malondialdehyde (MDA), and plasma tumor necrosis factor alpha (TNF-α) were significantly increased in l-NAME-hypertensive rats (p<0.05). This was consistent with up-regulation of the p47 NADPH oxidase subunit and iNOS protein expression in aortic tissues (p<0.05). Low levels of plasma nitric oxide metabolites were observed in l-NAME hypertension. GME prevented the development of hypertension and cardiovascular remodeling induced by l-NAME with reduced oxidative stress and inflammation. These data suggest that GME had a protective effect against l-NAME-induced hypertension and cardiovascular remodeling via suppressing p47 NADPH oxidase subunit and iNOS protein expression resulting in enhancing NO bioavailability.
[Mh] Termos MeSH primário: Sistema Cardiovascular/efeitos dos fármacos
Garcinia mangostana/química
Hipertensão/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Antioxidantes/farmacologia
Inibidores Enzimáticos/administração & dosagem
Inibidores Enzimáticos/efeitos adversos
Depuradores de Radicais Livres/metabolismo
Frutas/química
Hipertensão/induzido quimicamente
Hipertensão/complicações
Hipertensão/metabolismo
Hipertrofia Ventricular Esquerda/induzido quimicamente
Hipertrofia Ventricular Esquerda/etiologia
Hipertrofia Ventricular Esquerda/prevenção & controle
Inflamação/etiologia
Masculino
Artérias Mesentéricas/efeitos dos fármacos
Artérias Mesentéricas/patologia
NADPH Oxidases/antagonistas & inibidores
NADPH Oxidases/metabolismo
NG-Nitroarginina Metil Éster/administração & dosagem
NG-Nitroarginina Metil Éster/efeitos adversos
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Extratos Vegetais/uso terapêutico
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Remodelação Ventricular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Enzyme Inhibitors); 0 (Free Radical Scavengers); 0 (Plant Extracts); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (neutrophil cytosolic factor 1); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  5 / 11429 MEDLINE  
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[PMID]:28471497
[Au] Autor:Jacob CO; Yu N; Yoo DG; Perez-Zapata LJ; Barbu EA; Kaplan MJ; Purmalek M; Pingel JT; Idol RA; Dinauer MC
[Ad] Endereço:University of Southern California School of Medicine, Los Angeles.
[Ti] Título:Haploinsufficiency of NADPH Oxidase Subunit Neutrophil Cytosolic Factor 2 Is Sufficient to Accelerate Full-Blown Lupus in NZM 2328 Mice.
[So] Source:Arthritis Rheumatol;69(8):1647-1660, 2017 08.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We have previously established that the gene for neutrophil cytosolic factor 2 (NCF-2) predisposes to lupus, and we have identified lupus patients with point mutations that are predicted to cause reduced NADPH oxidase activity. We undertook this study to investigate the relationship between reduced leukocyte NADPH oxidase activity and immune dysregulation associated with systemic lupus erythematosus (SLE). METHODS: We generated NCF-2-null mice, in which NADPH oxidase activity is absent, on the nonautoimmune C57BL/6 (B6) mouse background and on the NZM 2328 mouse background, a polygenic model in which mice spontaneously develop lupus. Clinical disease, serology, and immunopathology were evaluated. RESULTS: NCF-2-null mice on the B6 background were susceptible to Aspergillus fumigatus pneumonia characteristic of chronic granulomatous disease, but did not develop systemic lupus disease. In contrast, NCF-2-null and even NCF-2-haploinsufficient mice on the NZM 2328 background developed accelerated full-blown lupus with significantly accelerated lupus kidney disease. This was characterized by more rapid development of hyperactive B cell and T cell immune compartments, increased expression of type I interferon-responsive genes, and generation of neutrophil extracellular traps, which were observed even in the absence of NADPH oxidase activity. CONCLUSION: Just as patients with chronic granulomatous disease who lack NADPH oxidase rarely develop SLE, NCF-2-null mice on a nonautoimmune background were susceptible to a chronic granulomatous disease-like opportunistic infection but did not develop lupus. In contrast, on a lupus-prone background, even haploinsufficiency of NCF-2 accelerated the development of full-blown lupus disease. This establishes an interaction between reduced oxidase activity and other lupus-predisposing genes, paralleling human SLE-associated variants predicted to have only reduced NADPH oxidase activity.
[Mh] Termos MeSH primário: Haploinsuficiência/genética
Lúpus Eritematoso Sistêmico/genética
Nefrite Lúpica/genética
NADPH Oxidases/genética
[Mh] Termos MeSH secundário: Animais
Aspergillus fumigatus
Linfócitos B/imunologia
Catelicidinas/imunologia
Progressão da Doença
Ensaio de Imunoadsorção Enzimática
Armadilhas Extracelulares/imunologia
Regulação da Expressão Gênica/imunologia
Predisposição Genética para Doença
Doença Granulomatosa Crônica/genética
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Rim/imunologia
Rim/patologia
Lúpus Eritematoso Sistêmico/imunologia
Nefrite Lúpica/imunologia
Nefrite Lúpica/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Aspergilose Pulmonar/genética
Reação em Cadeia da Polimerase em Tempo Real
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cathelicidins); 0 (Interferon Type I); 0 (cathelicidin antimicrobial peptide); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (Ncf2 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/art.40141


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[PMID]:29227594
[Au] Autor:Bazalii AV; Horak IR; Pasi chn yk GV; Komisarenko SV; Drobot LB
[Ti] Título:Transcriptional regulation of NOX genes express ion in human breast adenocarcinoma MCF-7 cells is modulated by adaptor protein Ruk/CIN 85.
[So] Source:Ukr Biochem J;88(1):119-25, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:NADPH oxidases are key components of redox-dependent signaling networks involved in the control of cancer cell proliferation, survival and invasion. The data have been accumulated that demonstrate specific expression patterns and levels of NADPH oxidase homologues (NOXs) and accessory genes in human cancer cell lines and primary tumors as well as modulation of these parameters by extracellular cues. Our previous studies revealed that ROS production by human colorectal adenocarcinoma HT-29 cells is positively correlated with adaptor protein Ruk/CIN85 expression while increased levels of Ruk/CIN85 in weakly invasive human breast adenocarcinoma MC F-7 cells contribute to their malignant phenotype through the constitutive activation of Src/Akt pathway. In this study, to investigate whether overexpression of Ruk/CIN85 in MC F-7 cells can influence transcriptional regulation of NOXs genes, the subclones of MCF-7 cells with different levels of Ruk/CIN85 were screened for NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2 as well as for regulatory subunit p22Phox mRNA contents by quantitative RT-PCR (qPCR). Systemic multidirectional changes in mRNA levels for NOX1, NOX2, NOX5, DUOX2 and p22Phox were revealed in Ruk/CIN85 overexpressing cells in comparison to control WT cells. Knocking down of Ruk/CIN85 using technology of RNA-interference resulted in the reversion of these changes. Further studies are necessary to elucidate, by which molecular mechanisms Ruk/CIN85 could affect transcriptional regulation of NOXs genes.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Regulação Neoplásica da Expressão Gênica
NADPH Oxidase 1/genética
Espécies Reativas de Oxigênio/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/antagonistas & inibidores
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Células Clonais
Oxidases Duais/genética
Oxidases Duais/metabolismo
Seres Humanos
Isoenzimas/genética
Isoenzimas/metabolismo
Células MCF-7
NADPH Oxidase 1/metabolismo
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Isoenzymes); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (SH3KBP1 protein, human); EC 1.11.1.- (Dual Oxidases); EC 1.6.3.- (NADPH Oxidase 1); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX1 protein, human); EC 1.6.3.1 (CYBA protein, human); EC 1.6.3.1 (DUOX1 protein, human); EC 1.6.3.1 (DUOX2 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.119


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[PMID]:29258552
[Au] Autor:Chavushyan VA; Simonyan KV; Simonyan RM; Isoyan AS; Simonyan GM; Babakhanyan MA; Hovhannisyian LE; Nahapetyan KH; Avetisyan LG; Simonyan MA
[Ad] Endereço:Orbeli Institute of Physiology NAS RA, 22 Orbeli Bros Street, 0028, Yerevan, Armenia.
[Ti] Título:Effects of stevia on synaptic plasticity and NADPH oxidase level of CNS in conditions of metabolic disorders caused by fructose.
[So] Source:BMC Complement Altern Med;17(1):540, 2017 Dec 19.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Excess dietary fructose intake associated with metabolic syndrome and insulin resistance and increased risk of developing type 2 diabetes. Previous animal studies have reported that diabetic animals have significantly impaired behavioural and cognitive functions, pathological synaptic function and impaired expression of glutamate receptors. Correction of the antioxidant status of laboratory rodents largely prevents the development of fructose-induced plurimetabolic changes in the nervous system. We suggest a novel concept of efficiency of Stevia leaves for treatment of central diabetic neuropathy. METHODS: By in vivo extracellular studies induced spike activity of hippocampal neurons during high frequency stimulation of entorhinal cortex, as well as neurons of basolateral amygdala to high-frequency stimulation of the hippocampus effects of Stevia rebaudiana Bertoni plant evaluated in synaptic activity in the brain of fructose-enriched diet rats. In the conditions of metabolic disorders caused by fructose, antioxidant activity of Stevia rebaudiana was assessed by measuring the NOX activity of the hippocampus, amygdala and spinal cord. RESULTS: In this study, the characteristic features of the metabolic effects of dietary fructose on synaptic plasticity in hippocampal neurons and basolateral amygdala and the state of the NADPH oxidase (NOX) oxidative system of these brain formations are revealed, as well as the prospects for development of multitarget and polyfunctional phytopreparations (with adaptogenic, antioxidant, antidiabetic, nootropic activity) from native raw material of Stevia rebaudiana. Stevia modulates degree of expressiveness of potentiation/depression (approaches but fails to achieve the norm) by shifting the percentage balance in favor of depressor type of responses during high-frequency stimulation, indicating its adaptogenic role in plasticity of neural networks. Under the action of fructose an increase (3-5 times) in specific quantity of total fraction of NOX isoforms isolated from the central nervous system tissue (amygdala, hippocampus, spinal cord) was revealed. Stevia exhibits an antistress, membrane-stabilizing role reducing the level of total fractions of NOX isoforms from central nervous system tissues and regulates NADPH-dependent O -producing activity. CONCLUSION: Generally, in condition of metabolic disorders caused by intensive consumption of dietary fructose Stevia leaves contributes to the control of neuronal synaptic plasticity possibly influencing the conjugated NOX-specific targets.
[Mh] Termos MeSH primário: Química Encefálica/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Diterpenos Caurânicos/farmacologia
Frutose/efeitos adversos
Glucosídeos/farmacologia
NADPH Oxidases/análise
Plasticidade Neuronal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Encéfalo/citologia
Encéfalo/enzimologia
Açúcares da Dieta/efeitos adversos
Masculino
Doenças Metabólicas/induzido quimicamente
Doenças Metabólicas/metabolismo
NADPH Oxidases/metabolismo
Ratos
Stevia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Sugars); 0 (Diterpenes, Kaurane); 0 (Glucosides); 0YON5MXJ9P (stevioside); 30237-26-4 (Fructose); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2049-9


  8 / 11429 MEDLINE  
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Carvalho, Denise P
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[PMID]:29180001
[Au] Autor:Bernardes JR; Faria CC; Andrade IS; Ferreira ACF; Carvalho DP; Leitão AC; de Alencar TAM; Fortunato RS
[Ad] Endereço:Laboratório de Radiobiologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:Effect of the FE chelation by 2,2'-dipyridyl in the doxorubicin-induced lethality in breast tumor cell lines.
[So] Source:Life Sci;192:128-135, 2018 Jan 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Breast cancer cells may exhibit changes in iron homeostasis, which results in increased labile iron pool (LIP) levels. Several studies highlight the crucial role of high LIP levels in the maintenance of tumor cell physiology. Iron chelators have been tested in anticancer therapy in combination with chemotherapeutic agents, to improve drug efficacy. Thus, the aim of this study was to evaluate the effect of 2,2'-dipyridyl (DIP), a Fe chelator, in combination with doxorubicin (DOX) in breast tumor cells. The maximum concentration of DIP that did not significantly reduce the viability of MDA-MB-231 cells was 10µM and for MCF-7 cells was 50µM. We observed that MCF-7 had higher LIP levels than MDA-MB-231 cells. DIP alone increased ROS generation in MCF-7 cells, and DIP pretreatment reduced ROS generation induced by DOX treatment. In conclusion, the increase in MCF-7 cell viability induced by DIP pretreatment in DOX-treated cells seems to be related to an increase in the cellular antioxidant capacity and the iron chelator did not improve drug efficacy in the two breast tumor cell lines analyzed.
[Mh] Termos MeSH primário: 2,2´-Dipiridil/farmacologia
Antibióticos Antineoplásicos/toxicidade
Neoplasias da Mama/tratamento farmacológico
Doxorrubicina/toxicidade
Quelantes de Ferro/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular
Sinergismo Farmacológico
Feminino
Seres Humanos
Células MCF-7
NADPH Oxidases/biossíntese
RNA Mensageiro/biossíntese
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Iron Chelating Agents); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 551W113ZEP (2,2'-Dipyridyl); 80168379AG (Doxorubicin); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


  9 / 11429 MEDLINE  
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[PMID]:28747378
[Au] Autor:Jha JC; Banal C; Okabe J; Gray SP; Hettige T; Chow BSM; Thallas-Bonke V; De Vos L; Holterman CE; Coughlan MT; Power DA; Skene A; Ekinci EI; Cooper ME; Touyz RM; Kennedy CR; Jandeleit-Dahm K
[Ad] Endereço:JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetic Complications Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
[Ti] Título:NADPH Oxidase Nox5 Accelerates Renal Injury in Diabetic Nephropathy.
[So] Source:Diabetes;66(10):2691-2703, 2017 10.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NADPH oxidase-derived excessive production of reactive oxygen species (ROS) in the kidney plays a key role in mediating renal injury in diabetes. Pathological changes in diabetes include mesangial expansion and accumulation of extracellular matrix (ECM) leading to glomerulosclerosis. There is a paucity of data about the role of the Nox5 isoform of NADPH oxidase in animal models of diabetic nephropathy since Nox5 is absent in the mouse genome. Thus, we examined the role of Nox5 in human diabetic nephropathy in human mesangial cells and in an inducible human Nox5 transgenic mouse exposed to streptozotocin-induced diabetes. In human kidney biopsies, Nox5 was identified to be expressed in glomeruli, which appeared to be increased in diabetes. Colocalization demonstrated Nox5 expression in mesangial cells. In vitro, silencing of Nox5 in human mesangial cells was associated with attenuation of the hyperglycemia and TGF-ß1-induced enhanced ROS production, increased expression of profibrotic and proinflammatory mediators, and increased TRPC6, PKC-α, and PKC-ß expression. In vivo, vascular smooth muscle cell/mesangial cell-specific overexpression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS production, accelerated glomerulosclerosis, mesangial expansion, and ECM protein (collagen IV and fibronectin) accumulation as well as increased macrophage infiltration and expression of the proinflammatory chemokine MCP-1. Collectively, this study provides evidence of a role for Nox5 and its derived ROS in promoting progression of diabetic nephropathy.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/metabolismo
NADPH Oxidases/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Nefropatias Diabéticas/genética
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Inflamação/metabolismo
Rim/metabolismo
Glomérulos Renais/metabolismo
Células Mesangiais/metabolismo
Camundongos
Camundongos Transgênicos
NADPH Oxidases/genética
Proteína Quinase C beta/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidases); EC 2.7.11.13 (Protein Kinase C beta)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1585


  10 / 11429 MEDLINE  
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[PMID]:29228045
[Au] Autor:Chao WC; Yen CL; Hsieh CY; Huang YF; Tseng YL; Nigrovic PA; Shieh CC
[Ad] Endereço:Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
[Ti] Título:Mycobacterial infection induces higher interleukin-1ß and dysregulated lung inflammation in mice with defective leukocyte NADPH oxidase.
[So] Source:PLoS One;12(12):e0189453, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Granulomatous inflammation causes severe tissue damage in mycobacterial infection while redox status was reported to be crucial in the granulomatous inflammation. Here, we used a NADPH oxidase 2 (NOX2)-deficient mice (Ncf1-/-) to investigate the role of leukocyte-produced reactive oxygen species (ROS) in mycobacterium-induced granulomatous inflammation. We found poorly controlled mycobacterial proliferation, significant body weight loss, and a high mortality rate after M. marinum infection in Ncf1-/- mice. Moreover, we noticed loose and neutrophilic granulomas and higher levels of interleukin (IL)-1ß and neutrophil chemokines in Ncf1-/- mice when compared with those in wild type mice. The lack of ROS led to reduced production of IL-1ß in macrophages, whereas neutrophil elastase (NE), an abundant product of neutrophils, may potentially exert increased inflammasome-independent protease activity and lead to higher IL-1ß production. Moreover, we showed that the abundant NE and IL-1ß were present in the caseous granulomatous inflammation of human TB infection. Importantly, blocking of IL-1ß with either a specific antibody or a recombinant IL-1 receptor ameliorated the pulmonary inflammation. These findings revealed a novel role of ROS in the early pathogenesis of neutrophilic granulomatous inflammation and suggested a potential role of IL-1 blocking in the treatment of mycobacterial infection in the lung.
[Mh] Termos MeSH primário: Interleucina-1beta/metabolismo
Leucócitos/enzimologia
Infecções por Mycobacterium/metabolismo
NADPH Oxidases/sangue
Pneumonia/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Infecções por Mycobacterium/enzimologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189453



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