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[PMID]:29334221
[Au] Autor:Liu L; Gong W; Sun X; Chen G; Wang L
[Ad] Endereço:State Key Laboratory of Microbial Technology, Shandong University , 27 Shandanan Road, Jinan 250100, China.
[Ti] Título:Extracellular Enzyme Composition and Functional Characteristics of Aspergillus niger An-76 Induced by Food Processing Byproducts and Based on Integrated Functional Omics.
[So] Source:J Agric Food Chem;66(5):1285-1295, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Byproducts of food processing can be utilized for the production of high-value-added enzyme cocktails. In this study, we utilized integrated functional omics technology to analyze composition and functional characteristics of extracellular enzymes produced by Aspergillus niger grown on food processing byproducts. The results showed that oligosaccharides constituted by arabinose, xylose, and glucose in wheat bran were able to efficiently induce the production of extracellular enzymes of A. niger. Compared with other substrates, wheat bran was more effective at inducing the secretion of ß-glucosidases from GH1 and GH3 families, as well as >50% of proteases from A1-family aspartic proteases. Compared with proteins induced by single wheat bran or soybean dregs, the protein yield induced by their mixture was doubled, and the time required to reach peak enzyme activity was shortened by 25%. This study provided a technical platform for the complex formulation of various substrates and functional analysis of extracellular enzymes.
[Mh] Termos MeSH primário: Aspergillus niger/enzimologia
Aspergillus niger/crescimento & desenvolvimento
Indução Enzimática/efeitos dos fármacos
Manipulação de Alimentos
Oligossacarídeos/farmacologia
Resíduos
[Mh] Termos MeSH secundário: Arabinose/farmacologia
Ácido Aspártico Proteases/biossíntese
Celulases/biossíntese
Fibras na Dieta/análise
Grãos Comestíveis/química
Fermentação
Glucose/farmacologia
Glicosídeo Hidrolases/biossíntese
Peptídeo Hidrolases/biossíntese
Xilose/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fiber); 0 (Oligosaccharides); 0 (Waste Products); A1TA934AKO (Xylose); B40ROO395Z (Arabinose); EC 3.2.1.- (Cellulases); EC 3.2.1.- (Glycoside Hydrolases); EC 3.4.- (Aspartic Acid Proteases); EC 3.4.- (Peptide Hydrolases); IY9XDZ35W2 (Glucose)
[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:180116
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b05164


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[PMID]:29329342
[Au] Autor:Ahmad M; Suhaimi SN; Chu TL; Abdul Aziz N; Mohd Kornain NK; Samiulla DS; Lo KW; Ng CH; Khoo AS
[Ad] Endereço:Molecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur, Malaysia.
[Ti] Título:Ternary copper(II) complex: NCI60 screening, toxicity studies, and evaluation of efficacy in xenograft models of nasopharyngeal carcinoma.
[So] Source:PLoS One;13(1):e0191295, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Copper(II) ternary complex, [Cu(phen)(C-dmg)(H2O)]NO3 was evaluated against a panel of cell lines, tested for in vivo efficacy in nasopharyngeal carcinoma xenograft models as well as for toxicity in NOD scid gamma mice. The Cu(II) complex displayed broad spectrum cytotoxicity against multiple cancer types, including lung, colon, central nervous system, melanoma, ovarian, and prostate cancer cell lines in the NCI-60 panel. The Cu(II) complex did not cause significant induction of cytochrome P450 (CYP) 3A and 1A enzymes but moderately inhibited CYP isoforms 1A2, 2C9, 2C19, 2D6, 2B6, 2C8 and 3A4. The complex significantly inhibited tumor growth in nasopharyngeal carcinoma xenograft bearing mice models at doses which were well tolerated without causing significant or permanent toxic side effects. However, higher doses which resulted in better inhibition of tumor growth also resulted in toxicity.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Carcinoma/tratamento farmacológico
Cobre/química
Neoplasias Nasofaríngeas/tratamento farmacológico
Compostos Organometálicos/química
Compostos Organometálicos/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/toxicidade
Carcinoma/patologia
Linhagem Celular Tumoral
Inibidores das Enzimas do Citocromo P-450/química
Inibidores das Enzimas do Citocromo P-450/farmacologia
Inibidores das Enzimas do Citocromo P-450/toxicidade
Sistema Enzimático do Citocromo P-450/biossíntese
Sistema Enzimático do Citocromo P-450/metabolismo
Relação Dose-Resposta a Droga
Indução Enzimática/efeitos dos fármacos
Feminino
Hepatócitos/efeitos dos fármacos
Camundongos
Neoplasias Nasofaríngeas/patologia
Compostos Organometálicos/toxicidade
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytochrome P-450 Enzyme Inhibitors); 0 (Organometallic Compounds); 789U1901C5 (Copper); 9035-51-2 (Cytochrome P-450 Enzyme System)
[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:180113
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191295


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[PMID]:29107029
[Au] Autor:Chen YY; Chan KM
[Ad] Endereço:School of Life Sciences, Faculty of Science, Chinese University, Sha Tin, Hong Kong.
[Ti] Título:Transcriptional inhibition of TCDD-mediated induction of cytochrome P450 1A1 and alteration of protein expression in a zebrafish hepatic cell line following the administration of TCDD and Cd .
[So] Source:Toxicol Lett;282:121-135, 2018 Jan 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We studied the effects of Cd on TCDD-mediated induction of the cytochrome P450 1A1 (cyp1a1) gene using a zebrafish liver cell line (ZFL). Our results showed that Cd inhibited the TCDD-mediated induction of the cyp1a1 protein, enzyme activity, and mRNA expression level. Cd also down-regulated levels of the aryl hydrocarbon receptor (ahr2) and the aryl hydrocarbon receptor nuclear translocator 2b (arnt2b) mRNAs. Compared with TCDD (3nM) treatment alone, co-treatment with Cd (0-30µM) and TCDD (3nM) significantly inhibited the activity of the luciferase reporter gene constructs harboring the distal promoter region (P-2626/-2009) of CYP1A1 and the synthetic 3XRE gene promoter. This indicates that Cd decreased the level of TCDD-induced cyp1a1 through transcriptional inhibition. Proteomic analysis was also used to evaluate the effect of Cd on TCDD-altered protein expression in ZFL cells. The identified proteins are mainly enzymes of the glycolysis pathway and proteasomes, and have anti-oxidative and anti-stress effects.
[Mh] Termos MeSH primário: Cloreto de Cádmio/toxicidade
Citocromo P-450 CYP1A1/biossíntese
Poluentes Ambientais/toxicidade
Expressão Gênica/efeitos dos fármacos
Fígado/efeitos dos fármacos
Dibenzodioxinas Policloradas/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Indução Enzimática
Fígado/enzimologia
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Polychlorinated Dibenzodioxins); 0 (Zebrafish Proteins); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); J6K4F9V3BA (Cadmium Chloride)
[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:171107
[St] Status:MEDLINE


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[PMID]:28419442
[Au] Autor:Arumugam B; Vairamani M; Partridge NC; Selvamurugan N
[Ad] Endereço:Department of Biotechnology, School of Bioengineering, SRM University, Kattankulathur, Tamil Nadu, India.
[Ti] Título:Characterization of Runx2 phosphorylation sites required for TGF-ß1-mediated stimulation of matrix metalloproteinase-13 expression in osteoblastic cells.
[So] Source:J Cell Physiol;233(2):1082-1094, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor-beta1 (TGF-ß1), a highly abundant growth factor in skeletal tissues, stimulates matrix metalloproteinase-13 (MMP-13) expression in osteoblastic cells. MMP-13 plays a critical role in bone remodeling. Runx2, a bone transcription factor, is required for TGF-ß1-mediated stimulation of MMP-13 expression in osteoblastic cells. In this study, the molecular mechanism responsible for TGF-ß1-stimulation of MMP-13 expression via Runx2 in osteoblastic cells was elucidated. TGF-ß1 stimulated the phosphorylation of Runx2 at serine amino acids, and ERK inhibition blocked this effect in rat (UMR106-01) and human (MG-63) osteoblastic cells. Pretreatment with okadaic acid, a serine-threonine phosphatase inhibitor, increased Runx2 serine phosphorylation in osteoblastic cells. When cells were pretreated with an ERK inhibitor, TGF-ß1-mediated stimulation of MMP-13 mRNA expression decreased. Nano-ESI/LC/MS analysis identified that TGF-ß1 stimulates Runx2 phosphorylation at three serine amino acids. Transient transfection of mouse mesenchymal stem cells (C3H10T1/2) with Runx2 serine mutant constructs decreased TGF-ß1-mediated Runx2 serine phosphorylation. A luciferase reporter assay identified that TGF-ß1 stimulated MMP-13 promoter activity in these cells only in the presence of the wild Runx2 construct, and not with mutant Runx2. Thus, TGF-ß1 stimulates the phosphorylation of Runx2 at three serine amino acids, and this event is required for MMP-13 expression in osteoblastic cells. Hence, this study contributes to the knowledge of events governing bone remodeling and bone-related diseases.
[Mh] Termos MeSH primário: Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Metaloproteinase 13 da Matriz/biossíntese
Osteoblastos/efeitos dos fármacos
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Animais
Remodelação Óssea/efeitos dos fármacos
Linhagem Celular
Subunidade alfa 1 de Fator de Ligação ao Core/genética
Indução Enzimática
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Metaloproteinase 13 da Matriz/genética
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/enzimologia
Camundongos Endogâmicos C3H
Mutação
Ácido Okadáico/farmacologia
Osteoblastos/enzimologia
Osteogênese/efeitos dos fármacos
Fosforilação
Regiões Promotoras Genéticas
Ratos
Transdução de Sinais/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Ativação Transcricional/efeitos dos fármacos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (RUNX2 protein, human); 0 (Runx2 protein, mouse); 0 (Runx2 protein, rat); 0 (Transforming Growth Factor beta1); 1W21G5Q4N2 (Okadaic Acid); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.24.- (MMP13 protein, human); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.- (Mmp13 protein, mouse); EC 3.4.24.- (Mmp13 protein, rat)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25964


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[PMID]:28935757
[Au] Autor:Moran CS; Biros E; Krishna SM; Wang Y; Tikellis C; Morton SK; Moxon JV; Cooper ME; Norman PE; Burrell LM; Thomas MC; Golledge J
[Ad] Endereço:From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Australia (C.S.M., E.B., S.M.K., S.K.M., J.V.M., J.G.); School of Applied and Biomedical Sciences, Faculty of Science and Technology, Fede
[Ti] Título:Resveratrol Inhibits Growth of Experimental Abdominal Aortic Aneurysm Associated With Upregulation of Angiotensin-Converting Enzyme 2.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2195-2203, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Recent evidence suggests an important role for angiotensin-converting enzyme 2 (ACE2) in limiting abdominal aortic aneurysm (AAA). This study examined the effect of ACE2 deficiency on AAA development and the efficacy of resveratrol to upregulate ACE2 in experimental AAA. APPROACH AND RESULTS: deletion in apolipoprotein-deficient mice ( ) resulted in increased aortic diameter and spontaneous aneurysm of the suprarenal aorta associated with increased expression of inflammation and proteolytic enzyme markers. In humans, serum ACE2 activity was negatively associated with AAA diagnosis. expression was lower in infrarenal biopsies of patients with AAA than organ donors. AAA was more severe in mice compared with controls in 2 experimental models. Resveratrol (0.05/100-g chow) inhibited growth of pre-established AAAs in mice fed high-fat chow and infused with angiotensin II continuously for 56 days. Reduced suprarenal aorta dilatation in mice receiving resveratrol was associated with elevated serum ACE2 and increased suprarenal aorta tissue levels of ACE2 and sirtuin 1 activity. In addition, the relative phosphorylation of Akt and ERK (extracellular signal-regulated kinase) 1/2 within suprarenal aorta tissue and gene expression for nuclear factor of kappa light polypeptide gene enhancer in B cells 1, angiotensin type-1 receptor, and metallopeptidase 2 and 9 were significantly reduced. Upregulation of ACE2 in human aortic smooth muscle cells by resveratrol in vitro was sirtuin 1-dependent. CONCLUSIONS: This study provides experimental evidence of an important role for ACE2 in limiting AAA development and growth. Resveratrol upregulated ACE2 and inhibited AAA growth in a mouse model.
[Mh] Termos MeSH primário: Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/prevenção & controle
Ruptura Aórtica/prevenção & controle
Peptidil Dipeptidase A/deficiência
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Angiotensina II
Animais
Aorta Abdominal/enzimologia
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/enzimologia
Aneurisma da Aorta Abdominal/genética
Aneurisma da Aorta Abdominal/patologia
Ruptura Aórtica/enzimologia
Ruptura Aórtica/genética
Ruptura Aórtica/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Células Cultivadas
Dieta Hiperlipídica
Dilatação Patológica
Modelos Animais de Doenças
Indução Enzimática
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Predisposição Genética para Doença
Seres Humanos
Mediadores da Inflamação/metabolismo
Camundongos Knockout
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/enzimologia
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Subunidade p50 de NF-kappa B/metabolismo
Peptidil Dipeptidase A/biossíntese
Peptidil Dipeptidase A/genética
Fenótipo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Sirtuína 1/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Inflammation Mediators); 0 (NF-kappa B p50 Subunit); 0 (Stilbenes); 11128-99-7 (Angiotensin II); 147257-52-1 (Nfkb1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.310129


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[PMID]:28916194
[Au] Autor:Rasmussen MK
[Ad] Endereço:Department of Food Science, Aarhus University, Blichers alle 20, DK-8830 Tjele, Denmark. Electronic address: Martink.rasmussen@food.au.dk.
[Ti] Título:Induction of cytochrome P450 mRNA in porcine primary hepatocytes cultured under serum free conditions: Comparison of freshly isolated cells and cryopreserved.
[So] Source:Exp Cell Res;360(2):218-225, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary hepatocytes are widely used in the study of dynamic events like regulation of gene expression, as they are superior to most cell-lines. However, the culturing of the hepatocytes often results in loss of phenotype, e.g. the expression of the cytochrome p450s (CYP). The present study investigated the impact of serum in the culture medium of porcine primary hepatocytes (PPH) on markers of dedifferentiation as well as the impact on CYP induction. The effects were studied in both freshly isolated primary hepatocytes as well as cryopreserved. The exclusion of serum in the culturing media were not introducing significant dedifferentiation as judged by the gene expression of α-fetoprotein, albumin, glucose-6-phosphatase and the constitutive expression of selected transcription factors and CYP. The induction of CYP2B22 and CYP3A29 by phenobarbital and rifampicin, were greater in hepatocytes cultured without serum. The same were not observed for TCDD induced CYP1A2 expression. In conclusion, PPH cultured under serum free conditions results in little or no dedifferentiation, while being more responsive to known CYP inducers. Hence, it can be suggested that PPH cultured under serum free conditions provides a reliable hepatocyte model to investigate CYP gene regulation.
[Mh] Termos MeSH primário: Meios de Cultura Livres de Soro/farmacologia
Sistema Enzimático do Citocromo P-450/genética
Hepatócitos/citologia
Hepatócitos/metabolismo
Cultura Primária de Células/métodos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Criopreservação
Sistema Enzimático do Citocromo P-450/metabolismo
Indução Enzimática
Feminino
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Hepatócitos/efeitos dos fármacos
Hepatócitos/enzimologia
RNA Mensageiro/metabolismo
Manejo de Espécimes/métodos
Suínos
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Serum-Free); 0 (RNA, Messenger); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE


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[PMID]:28893642
[Au] Autor:Jiang B; Meng L; Zhang F; Jin X; Zhang G
[Ad] Endereço:Department of Pharmacy, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. Electronic address: Lucid1227@163.com.
[Ti] Título:Enzyme-inducing effects of berberine on cytochrome P450 1A2 in vitro and in vivo.
[So] Source:Life Sci;189:1-7, 2017 Nov 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Berberine (BER) is an important anti-bacterial drug from Chinese herbal medicine and a novel drug candidate for preclinical development in recent years. Here we provide evidence that the effects of berberine on cytochrome P450 (CYP) 1A2 in vitro and in vivo. MAIN METHODS: Real-time polymerase chain reaction and western blotting analysis were employed to evaluate the CYP1A2 mRNA levels and protein expression. The enzyme activity was assessed by the metabolic rate of phenacetin to acetaminophen by LC-MS/MS method. KEY FINDINGS: The results indicated that the CYP1A2 mRNA expression and enzyme activity in HepG2 cells after treated with BER (4.5µg/ml) exhibited a significant induction (16.11-fold and 5.0-fold, respectively), which was consistent with those on rat liver microsomes (4.5-fold and 1.98-fold, respectively) by BER induction (10mg/kg/day, i.p.) ex vivo. Beside, BER induced CYP1A2 activity with increases in AUC and C of acetaminophen and the Ke and t of phenacetin after oral administration of phenacetin (p<0.05) in vivo. SIGNIFICANCE: This study firstly reported the induction effect of BER on rats CYP1A2 by intraperitoneal route. But, BER didn't show significant induction effect on CYP1A2 by high-dose orally administrating to rats for 6 consecutive days due to the extremely low bioavailability. The potential drug-drug interactions were supposed to happen when the liver exposed to high dose of BER in vivo by changing administration route.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Berberina/farmacologia
Citocromo P-450 CYP1A2/efeitos dos fármacos
Indução Enzimática/efeitos dos fármacos
Fenacetina/farmacocinética
[Mh] Termos MeSH secundário: Acetaminofen/farmacocinética
Animais
Área Sob a Curva
Western Blotting
Cromatografia Líquida/métodos
Citocromo P-450 CYP1A2/biossíntese
Meia-Vida
Células Hep G2
Seres Humanos
Masculino
Microssomos Hepáticos/efeitos dos fármacos
Microssomos Hepáticos/metabolismo
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (RNA, Messenger); 0I8Y3P32UF (Berberine); 362O9ITL9D (Acetaminophen); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); ER0CTH01H9 (Phenacetin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE


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[PMID]:28882872
[Au] Autor:Feng S; Bowden N; Fragiadaki M; Souilhol C; Hsiao S; Mahmoud M; Allen S; Pirri D; Ayllon BT; Akhtar S; Thompson AAR; Jo H; Weber C; Ridger V; Schober A; Evans PC
[Ad] Endereço:From the Department of Infection, Immunity, and Cardiovascular Disease, INSIGNEO Institute for In Silico Medicine, and the Bateson Centre (S.F., N.B., M.F., C.S., H.S., M.M., D.P., B.T.A., A.A.R.T., V.R., P.C.E.) and Sheffield Institute for Translational Neuroscience (S.A.), University of Sheffield,
[Ti] Título:Mechanical Activation of Hypoxia-Inducible Factor 1α Drives Endothelial Dysfunction at Atheroprone Sites.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2087-2101, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Atherosclerosis develops near branches and bends of arteries that are exposed to low shear stress (mechanical drag). These sites are characterized by excessive endothelial cell (EC) proliferation and inflammation that promote lesion initiation. The transcription factor HIF1α (hypoxia-inducible factor 1α) is canonically activated by hypoxia and has a role in plaque neovascularization. We studied the influence of shear stress on HIF1α activation and the contribution of this noncanonical pathway to lesion initiation. APPROACH AND RESULTS: Quantitative polymerase chain reaction and en face staining revealed that HIF1α was expressed preferentially at low shear stress regions of porcine and murine arteries. Low shear stress induced HIF1α in cultured EC in the presence of atmospheric oxygen. The mechanism involves the transcription factor nuclear factor-κB that induced HIF1α transcripts and induction of the deubiquitinating enzyme Cezanne that stabilized HIF1α protein. Gene silencing revealed that HIF1α enhanced proliferation and inflammatory activation in EC exposed to low shear stress via induction of glycolysis enzymes. We validated this observation by imposing low shear stress in murine carotid arteries (partial ligation) that upregulated the expression of HIF1α, glycolysis enzymes, and inflammatory genes and enhanced EC proliferation. EC-specific genetic deletion of HIF1α in hypercholesterolemic apolipoprotein E-defecient mice reduced inflammation and endothelial proliferation in partially ligated arteries, indicating that HIF1α drives inflammation and vascular dysfunction at low shear stress regions. CONCLUSIONS: Mechanical low shear stress activates HIF1α at atheroprone regions of arteries via nuclear factor-κB and Cezanne. HIF1α promotes atherosclerosis initiation at these sites by inducing excessive EC proliferation and inflammation via the induction of glycolysis enzymes.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Células Endoteliais/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Inflamação/metabolismo
Mecanotransdução Celular
Placa Aterosclerótica
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/patologia
Proliferação Celular
Células Cultivadas
Modelos Animais de Doenças
Endopeptidases/metabolismo
Células Endoteliais/patologia
Indução Enzimática
Feminino
Predisposição Genética para Doença
Glicólise
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Inflamação/genética
Inflamação/patologia
Mediadores da Inflamação/metabolismo
Camundongos Knockout
NF-kappa B/metabolismo
Oxigênio/metabolismo
Fenótipo
Estabilidade Proteica
Proteólise
Interferência de RNA
Fluxo Sanguíneo Regional
Estresse Mecânico
Sus scrofa
Fatores de Tempo
Transfecção
Ubiquitinação
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (HIF1A protein, human); 0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Inflammation Mediators); 0 (NF-kappa B); EC 3.4.- (Endopeptidases); EC 3.4.- (Otud7b protein, mouse); S88TT14065 (Oxygen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309249


  9 / 32236 MEDLINE  
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[PMID]:28830811
[Au] Autor:Vanle BC; Florang VR; Murry DJ; Aguirre AL; Doorn JA
[Ad] Endereço:Department of Pharmaceutical Sciences and Experimental Therapeutics, Division of Medicinal and Natural Products Chemistry, College of Pharmacy, The University of Iowa, 115 South Grand Ave, Iowa City, IA 52242-1112, United States.
[Ti] Título:Inactivation of glyceraldehyde-3-phosphate dehydrogenase by the dopamine metabolite, 3,4-dihydroxyphenylacetaldehyde.
[So] Source:Biochem Biophys Res Commun;492(2):275-281, 2017 Oct 14.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aldehyde metabolite of dopamine, 3,4-dihydroxyphenylacetaldehyde (DOPAL) is an endogenous neurotoxin implicated in Parkinson's Disease. Elucidating protein targets of DOPAL is essential in understanding it's pathology. The enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a target of DOPAL. METHODS: GAPDH activity was measured via reduction of NAD cofactor (340 nm). Protein aggregation was assessed with SDS-PAGE methods and specific modification via chemical probes. RESULTS: Low micromolar levels of DOPAL caused extensive GAPDH aggregation and irreversibly inhibited enzyme activity. The inactivation of GAPDH was dependent on both the catechol and aldehyde moieties of DOPAL. It is suggested that Cys are modified and oxidized by DOPAL. CONCLUSIONS: The mechanism by which DOPAL modifies GAPDH can serve as a mechanistic explanation to the pathological events in Parkinson's Disease.
[Mh] Termos MeSH primário: Ácido 3,4-Di-Hidroxifenilacético/análogos & derivados
Gliceraldeído-3-Fosfato Desidrogenases/metabolismo
[Mh] Termos MeSH secundário: Ácido 3,4-Di-Hidroxifenilacético/metabolismo
Animais
Dopamina/metabolismo
Indução Enzimática
Gliceraldeído-3-Fosfato Desidrogenases/química
Seres Humanos
Doença de Parkinson/metabolismo
Agregados Proteicos
Coelhos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Aggregates); 102-32-9 (3,4-Dihydroxyphenylacetic Acid); 5707-55-1 (3,4-dihydroxyphenylacetaldehyde); EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


  10 / 32236 MEDLINE  
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[PMID]:28828965
[Au] Autor:Liu Y; Kurita A; Nakashima S; Zhu B; Munemasa S; Nakamura T; Murata Y; Nakamura Y
[Ad] Endereço:a Graduate School of Environmental and Life Science , Okayama University , Okayama , Japan.
[Ti] Título:3,4-Dihydroxyphenylacetic acid is a potential aldehyde dehydrogenase inducer in murine hepatoma Hepa1c1c7 cells.
[So] Source:Biosci Biotechnol Biochem;81(10):1978-1983, 2017 Oct.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:3,4-Dihydroxyphenylacetic acid (DOPAC) is one of the major colonic microflora-produced catabolites of quercetin glycosides, such as quercetin 4'-glucoside derived from onion. Here, we investigated whether DOPAC modulates the aldehyde dehydrogenase (ALDH) activity and protects the cells from the acetaldehyde-induced cytotoxicity in vitro. DOPAC was shown to enhance not only the total ALDH activity, but also the gene expression of ALDH1A1, ALDH2 and ALDH3A1 in a concentration-dependent manner. DOPAC simultaneously stimulated the nuclear translocation of NFE2-related factor 2 and aryl hydrocarbon receptor. The pretreatment of DOPAC completely protected the cells from the acetaldehyde-induced cytotoxicity. The present study suggested that DOPAC acts as a potential ALDH inducer to prevent the alcohol-induced abnormal reaction.
[Mh] Termos MeSH primário: Ácido 3,4-Di-Hidroxifenilacético/farmacologia
Aldeído Desidrogenase/biossíntese
Carcinoma Hepatocelular/patologia
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Acetaldeído/toxicidade
Aldeído Desidrogenase/genética
Aldeído Desidrogenase/metabolismo
Animais
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Indução Enzimática/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
102-32-9 (3,4-Dihydroxyphenylacetic Acid); EC 1.2.1.3 (Aldehyde Dehydrogenase); GO1N1ZPR3B (Acetaldehyde)
[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:170823
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1361809



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