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[PMID]:29376560
[Au] Autor:Schumann J; Henrich EC; Strobl H; Prondzinsky R; Weiche S; Thiele H; Werdan K; Frantz S; Unverzagt S
[Ad] Endereço:Department of Anaesthesiology and Surgical Intensive Care, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany.
[Ti] Título:Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome.
[So] Source:Cochrane Database Syst Rev;1:CD009669, 2018 01 29.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cardiogenic shock (CS) and low cardiac output syndrome (LCOS) as complications of acute myocardial infarction (AMI), heart failure (HF) or cardiac surgery are life-threatening conditions. While there is a broad body of evidence for the treatment of people with acute coronary syndrome under stable haemodynamic conditions, the treatment strategies for people who become haemodynamically unstable or develop CS remain less clear. We have therefore summarised here the evidence on the treatment of people with CS or LCOS with different inotropic agents and vasodilative drugs. This is the first update of a Cochrane review originally published in 2014. OBJECTIVES: To assess efficacy and safety of cardiac care with positive inotropic agents and vasodilator strategies in people with CS or LCOS due to AMI, HF or cardiac surgery. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase and CPCI-S Web of Science in June 2017. We also searched four registers of ongoing trials and scanned reference lists and contacted experts in the field to obtain further information. No language restrictions were applied. SELECTION CRITERIA: Randomised controlled trials in people with myocardial infarction, heart failure or cardiac surgery complicated by cardiogenic shock or LCOS. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by Cochrane. MAIN RESULTS: We identified 13 eligible studies with 2001 participants (mean or median age range 58 to 73 years) and two ongoing studies. We categorised studies into eight comparisons, all against cardiac care and additional other active drugs or placebo. These comparisons investigated the efficacy of levosimendan versus dobutamine, enoximone or placebo, epinephrine versus norepinephrine-dobutamine, amrinone versus dobutamine, dopexamine versus dopamine, enoximone versus dopamine and nitric oxide versus placebo.All trials were published in peer-reviewed journals, and analysis was done by the intention-to-treat (ITT) principle. Twelve of 13 trials were small with few included participants. Acknowledgement of funding by the pharmaceutical industry or missing conflict of interest statements emerged in five of 13 trials. In general, confidence in the results of analysed studies was reduced due to serious study limitations, very serious imprecision or indirectness. Domains of concern, which show a high risk of more than 50%, include performance bias (blinding of participants and personnel) and bias affecting the quality of evidence on adverse events.Levosimendan may reduce short-term mortality compared to a therapy with dobutamine (RR 0.60, 95% CI 0.37 to 0.95; 6 studies; 1776 participants; low-quality evidence; NNT: 16 (patients with moderate risk), NNT: 5 (patients with CS)). This initial short-term survival benefit with levosimendan vs. dobutamine is not confirmed on long-term follow up. There is uncertainty (due to lack of statistical power) as to the effect of levosimendan compared to therapy with placebo (RR 0.48, 95% CI 0.12 to 1.94; 2 studies; 55 participants, very low-quality evidence) or enoximone (RR 0.50, 95% CI 0.22 to 1.14; 1 study; 32 participants, very low-quality evidence).All comparisons comparing other positive inotropic, inodilative or vasodilative drugs presented uncertainty on their effect on short-term mortality with very low-quality evidence and based on only one RCT. These single studies compared epinephrine with norepinephrine-dobutamine (RR 1.25, 95% CI 0.41 to 3.77; 30 participants), amrinone with dobutamine (RR 0.33, 95% CI 0.04 to 2.85; 30 participants), dopexamine with dopamine (no in-hospital deaths from 70 participants), enoximone with dobutamine (two deaths from 40 participants) and nitric oxide with placebo (one death from three participants). AUTHORS' CONCLUSIONS: Apart from low quality of evidence data suggesting a short-term mortality benefit of levosimendan compared with dobutamine, at present there are no robust and convincing data to support a distinct inotropic or vasodilator drug-based therapy as a superior solution to reduce mortality in haemodynamically unstable people with cardiogenic shock or LCOS.Considering the limited evidence derived from the present data due to a generally high risk of bias and imprecision, it should be emphasised that there remains a great need for large, well-designed randomised trials on this topic to close the gap between daily practice in critical care medicine and the available evidence. It seems to be useful to apply the concept of 'early goal-directed therapy' in cardiogenic shock and LCOS with early haemodynamic stabilisation within predefined timelines. Future clinical trials should therefore investigate whether such a therapeutic concept would influence survival rates much more than looking for the 'best' drug for haemodynamic support.
[Mh] Termos MeSH primário: Baixo Débito Cardíaco/tratamento farmacológico
Cardiotônicos/uso terapêutico
Infarto do Miocárdio/complicações
Choque Cardiogênico/tratamento farmacológico
Vasodilatadores/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Baixo Débito Cardíaco/etiologia
Baixo Débito Cardíaco/mortalidade
Causas de Morte
Dobutamina/uso terapêutico
Enoximona/uso terapêutico
Seres Humanos
Hidrazonas/uso terapêutico
Meia-Idade
Infarto do Miocárdio/mortalidade
Óxido Nítrico/uso terapêutico
Piridazinas/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Choque Cardiogênico/etiologia
Choque Cardiogênico/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Hydrazones); 0 (Pyridazines); 0 (Vasodilator Agents); 31C4KY9ESH (Nitric Oxide); 349552KRHK (simendan); 3S12J47372 (Dobutamine); C7Z4ITI7L7 (Enoximone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD009669.pub3


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[PMID]:29331754
[Au] Autor:Wang W; Xu S; Duan Y; Liu X; Li X; Wang C; Zhao B; Zheng P; Zhu W
[Ad] Endereço:Jiangxi Provincial Key Laboratory of Drug Design and Evaluation, School of Pharmacy, Jiangxi Science & Technology Normal University, Nanchang 330013, PR China.
[Ti] Título:Synthesis and bioevaluation and doking study of 1H-pyrrolo[2,3-b]pyridine derivatives bearing aromatic hydrazone moiety as c-Met inhibitors.
[So] Source:Eur J Med Chem;145:315-327, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Two series of aromatic hydrazone derivatives bearing 1H-pyrrolo[2,3-b]pyridine moiety (7a-r, 8a-i, 12a-b, 13a-c, 16a-d and 17a-e) were designed, synthesized and evaluated for the IC values against four cancer cell lines (A549, HepG2, MCF-7and PC-3). Two selected compounds (7c and 17e) were further evaluated for the activity against c-Met, Flt-3, VEGFR-2 and EGFR kinases. The data indicated that targets compounds were selective for c-Met kinase. And the most promising compound 7c was further studied in terms of dose-dependent, time-dependent and cell apoptosis. Most of the compounds showed excellent cytotoxicity activity, especially the most promising compound 7c with the IC values of 0.82 ±â€¯0.08 µM, 1.00 ±â€¯0.11 µM, 0.93 ±â€¯0.28 µM and 0.92 ±â€¯0.17 µM against A549, HepG2, MCF-7 and PC-3 cell lines and 0.506 µM against c-Met kinase. Structure-activity relationships (SARs) and docking studies indicated that the activities of the phenyl hydrazone derivatives (7a-r and 8a-i) were superior to that of the heterocyclic hydrazone series (12a-b, 13a-c, 16a-d and 17a-e). What's more, the further studies indicated that the target compounds can induce apoptosis of A549 cells and arrest efficiently the cell cycle progression in G2/M phase of A549 cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Hidrazonas/farmacologia
Simulação de Acoplamento Molecular
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores
Piridinas/farmacologia
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Hidrazonas/química
Estrutura Molecular
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Proteínas Proto-Oncogênicas c-met/metabolismo
Piridinas/síntese química
Piridinas/química
Pirróis/síntese química
Pirróis/química
Relação Estrutura-Atividade
Fatores de Tempo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hydrazones); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Pyrroles); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); QX4465NR9T (pyrrolo(2, 3-b)pyridine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


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[PMID]:29317633
[Au] Autor:Guo P; Liu D; Subramanyam K; Wang B; Yang J; Huang J; Auguste DT; Moses MA
[Ad] Endereço:Vascular Biology Program, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA.
[Ti] Título:Nanoparticle elasticity directs tumor uptake.
[So] Source:Nat Commun;9(1):130, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To date, the role of elasticity in drug delivery remains elusive due to the inability to measure microscale mechanics and alter rheology without affecting chemistry. Herein, we describe the in vitro cellular uptake and in vivo tumor uptake of nanolipogels (NLGs). NLGs are composed of identical lipid bilayers encapsulating an alginate core, with tunable elasticity. The elasticity of NLGs was evaluated by atomic force microscopy, which demonstrated that they exhibit Young's moduli ranging from 45 ± 9 to 19,000 ± 5 kPa. Neoplastic and non-neoplastic cells exhibited significantly greater uptake of soft NLGs (Young's modulus <1.6 MPa) relative to their elastic counterparts (Young's modulus >13.8 MPa). In an orthotopic breast tumor model, soft NLGs accumulated significantly more in tumors, whereas elastic NLGs preferentially accumulated in the liver. Our findings demonstrate that particle elasticity directs tumor accumulation, suggesting that it may be a design parameter to enhance tumor delivery efficiency.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Módulo de Elasticidade
Nanopartículas/química
Nanopartículas/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Linhagem Celular
Linhagem Celular Tumoral
Clorpromazina/farmacologia
Endocitose/efeitos dos fármacos
Filipina/farmacologia
Seres Humanos
Hidrazonas/farmacologia
Fígado/metabolismo
Células MCF-7
Neoplasias Mamárias Experimentais/metabolismo
Camundongos Endogâmicos BALB C
Microscopia de Força Atômica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydrazones); 0 (N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide); 87Z59R7D14 (Filipin); U42B7VYA4P (Chlorpromazine)
[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:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02588-9


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[PMID]:27770407
[Au] Autor:Li S; Fu S; Xiao Y; Xu G
[Ad] Endereço:Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.
[Ti] Título:Recent Perioperative Pharmacological Prevention of Acute Kidney Injury after Cardiac Surgery: A Narrative Review.
[So] Source:Am J Cardiovasc Drugs;17(1):17-25, 2017 Feb.
[Is] ISSN:1179-187X
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) is a common and severe complication of cardiac surgery, and related rates of both hospitalization and long-term mortality are increasing. A number of studies have explored the preventive effects of perioperative pharmacological therapy on AKI after cardiac surgery. However, the mechanisms of AKI are multifaceted, and no universal treatment has been confirmed as beneficial. We review and analyze several current perioperative pharmacological therapies for AKI after cardiac surgery to identify promising preventive strategies.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Procedimentos Cirúrgicos Cardíacos/efeitos adversos
Assistência Perioperatória/métodos
Complicações Pós-Operatórias/prevenção & controle
[Mh] Termos MeSH secundário: Lesão Renal Aguda/etiologia
Lesão Renal Aguda/metabolismo
Dexmedetomidina/uso terapêutico
Seres Humanos
Hidrazonas/uso terapêutico
Complicações Pós-Operatórias/etiologia
Complicações Pós-Operatórias/metabolismo
Piridazinas/uso terapêutico
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hydrazones); 0 (Pyridazines); 349552KRHK (simendan); 67VB76HONO (Dexmedetomidine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s40256-016-0194-z


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[PMID]:27775155
[Au] Autor:Angelova V; Karabeliov V; Andreeva-Gateva PA; Tchekalarova J
[Ad] Endereço:Department of Chemistry Faculty of Pharmacy, MU-Sofia, Sofia, Bulgaria.
[Ti] Título:Recent Developments of Hydrazide/Hydrazone Derivatives and Their Analogs as Anticonvulsant Agents in Animal Models.
[So] Source:Drug Dev Res;77(7):379-392, 2016 11.
[Is] ISSN:1098-2299
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preclinical Research Epilepsy is a chronic devastating neurological disorder characterized by synchronous interictal discharges. Treatment with antiepileptic drugs (AEDs) can alleviate spontaneous seizure activity without preventing the progression and development of epileptogenesis. Current design and development of new AEDs and strategies for the prevention of epilepsy is focused mainly on attenuating uncontrolled seizures, severe side effects and toxicity in chronic drug therapy. It has thus become necessary to discover new chemical pharmacophores with a broad spectrum of activity and less neurotoxicity. Hydrazide/hydrazone derivatives that possess a -CO-NHN=CH- group constitute an important class of compounds for drug development. This review highlights the specific characteristics of various hydrazide/hydrazone derivatives and structurally related semicarbazones, semicarbazides and Schiff base compounds and their anticonvulsant activities. It is focused on the influence of differently substituted pharmacophores developed through SAR studies and testing their activity against different pharmcological targets. Drug Dev Res 77 : 379-392, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Anticonvulsivantes/uso terapêutico
Epilepsia/tratamento farmacológico
Hidrazonas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/efeitos adversos
Anticonvulsivantes/química
Modelos Animais de Doenças
Desenho de Drogas
Epilepsia/fisiopatologia
Seres Humanos
Hidrazonas/efeitos adversos
Hidrazonas/química
Bases de Schiff/efeitos adversos
Bases de Schiff/química
Bases de Schiff/uso terapêutico
Semicarbazidas/efeitos adversos
Semicarbazidas/química
Semicarbazidas/uso terapêutico
Semicarbazonas/efeitos adversos
Semicarbazonas/química
Semicarbazonas/uso terapêutico
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Hydrazones); 0 (Schiff Bases); 0 (Semicarbazides); 0 (Semicarbazones)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/ddr.21329


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[PMID]:29208359
[Au] Autor:Dantas N; de Aquino TM; de Araújo-Júnior JX; da Silva-Júnior E; Gomes EA; Gomes AAS; Siqueira-Júnior JP; Mendonça Junior FJB
[Ad] Endereço:Laboratório de Genética de Microorganismo, Departamento de Biologia Molecular/CCEN/Universidade Federal da Paraíba-UFPB, 58051-970 João Pessoa, PB, Brazil.
[Ti] Título:Aminoguanidine hydrazones (AGH's) as modulators of norfloxacin resistance in Staphylococcus aureus that overexpress NorA efflux pump.
[So] Source:Chem Biol Interact;280:8-14, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:One of the promising fields for improving the effectiveness of antimicrobial agents is their combination with efflux pump inhibitors (EPIs), which besides expanding the use of existing antibiotics. The goal of this research was to evaluate a series of aminoguanidine hydrazones (AGH's, 1-19) as antibacterial agents and NorA efflux pump inhibitors in Staphylococcus aureus strain SA-1199B. Molecular modeling and docking studies were also performed in order to explain at the molecular level the interactions of the compounds with the generated NorA efflux pump model. The MICs of the antibiotic and ethidium bromide were determined by microdilution assay in absence or presence of a subinhibitory concentration of aminoguanidine hydrazones and macrophages viability was determined through MTT assay. Bioinformatic software Swiss-Model and AutoDock 4.2 were used to perform modeling and docking studies, respectively. As results, all AGH's were able to potentiate the action for the antibiotic norfloxacin, causing MIC's reduction of 16-fold and 32-fold to ethidium bromide. In the cell viability test, the concentration of 10 µg/mL showed better results than 90% and the concentration of 1000 µg/mL showed the lowest viability, reaching a maximum of 50% for the analyzed aminoguanidine hydrazones. Molecular docking studies showed that both norfloxacin and derivative 13 were recognized by the same binding site of NorA pump, suggesting a competitive mechanism. The present work demonstrated for the first time that AGH derivatives have potential to be putative inhibitors of NorA efflux pump, showing a promising activity as an antibacterial drug development.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Proteínas de Bactérias/metabolismo
Farmacorresistência Bacteriana/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Hidrazonas/química
Proteínas Associadas à Resistência a Múltiplos Medicamentos/metabolismo
Staphylococcus aureus/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/antagonistas & inibidores
Sítios de Ligação
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Inibidores Enzimáticos/química
Inibidores Enzimáticos/toxicidade
Guanidinas/química
Hidrazonas/síntese química
Hidrazonas/farmacologia
Camundongos
Testes de Sensibilidade Microbiana
Simulação de Acoplamento Molecular
Proteínas Associadas à Resistência a Múltiplos Medicamentos/antagonistas & inibidores
Norfloxacino/farmacologia
Estrutura Terciária de Proteína
Staphylococcus aureus/efeitos dos fármacos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Enzyme Inhibitors); 0 (Guanidines); 0 (Hydrazones); 0 (Multidrug Resistance-Associated Proteins); N0F8P22L1P (Norfloxacin); SCQ4EZQ113 (pimagedine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:29179200
[Au] Autor:Rinné S; Kiper AK; Schmidt C; Ortiz-Bonnin B; Zwiener S; Seebohm G; Decher N
[Ad] Endereço:Institute of Physiology and Pathophysiology, Vegetative Physiology, University of Marburg, Marburg, Germany.
[Ti] Título:Stress-Kinase Regulation of TASK-1 and TASK-3.
[So] Source:Cell Physiol Biochem;44(3):1024-1037, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: TASK channels belong to the two-pore-domain potassium (K2P) channel family. TASK-1 is discussed to contribute to chronic atrial fibrillation (AFib) and has been together with uncoupling protein 1 found as a marker protein of brown adipose tissue (BAT) fat. In addition, TASK-1 was linked in a genome-wide association study to an increased body mass index. A recent study showed that TASK-1 inhibition is causing obesity in mice by a BAT whitening and that these effects are linked to the mineralocorticoid receptor pathway, albeit the mechanism remained elusive. Therefore, we aimed to probe whether K2P channels are regulated by serum- and glucocorticoid-inducible kinases (SGKs) which are known to modify many cellular functions by modulating ion channels. METHODS: To this end we used functional co-expression studies and chemiluminescence-assays in Xenopus oocytes, together with fluorescence imaging and quantitative PCR experiments. RESULTS: SGKs and proteinkinase B (PKB) induced a strong, dose- and time-dependent current reduction of TASK-1 and TASK-3. SGK co-expression reduced the surface expression of TASK-1/3, leading to a predominant localization of the channels into late endosomes. The down regulation of TASK-3 channels was abrogated by the dynamin inhibitor dynasore, confirming a role of SGKs in TASK-1/3 channel endocytosis. CONCLUSION: Stress-mediated changes in SGK expression pattern or activation is likely to alter TASK-1/3 expression at the surface membrane. The observed TASK-1 regulation might contribute to the pathogenesis of chronic AFib and provide a mechanistic link between increased mineralocorticoid levels and TASK-1 reduction, both linked to BAT whitening.
[Mh] Termos MeSH primário: Proteínas do Tecido Nervoso/metabolismo
Canais de Potássio de Domínios Poros em Tandem/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/metabolismo
Animais
Células COS
Cercopithecus aethiops
Clatrina/metabolismo
Endocitose
Endossomos/metabolismo
Células HeLa
Seres Humanos
Hidrazonas/farmacologia
Proteínas Imediatamente Precoces/genética
Proteínas Imediatamente Precoces/metabolismo
Medições Luminescentes
Microscopia de Fluorescência
Proteínas do Tecido Nervoso/genética
Oócitos/química
Oócitos/fisiologia
Técnicas de Patch-Clamp
Plasmídeos/genética
Plasmídeos/metabolismo
Canais de Potássio de Domínios Poros em Tandem/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Imagem com Lapso de Tempo
Xenopus laevis/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Clathrin); 0 (Hydrazones); 0 (Immediate-Early Proteins); 0 (KCNK9 protein, human); 0 (N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide); 0 (Nerve Tissue Proteins); 0 (Potassium Channels, Tandem Pore Domain); 0 (potassium channel subfamily K member 3); EC 2.7.11.1 (3-Phosphoinositide-Dependent Protein Kinases); EC 2.7.11.1 (PDPK1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
[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:10.1159/000485402


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[PMID]:29175207
[Au] Autor:Shen F; Gai J; Xing J; Guan J; Fu L; Li Q
[Ad] Endereço:Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, China.
[Ti] Título:Dynasore suppresses proliferation and induces apoptosis of the non-small-cell lung cancer cell line A549.
[So] Source:Biochem Biophys Res Commun;495(1):1158-1166, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the leading cause of cancer death worldwide, and most of all cases are non-small-cell lung cancer. Lung cancer is associated with dysregulation of mitochondrial fusion and fission, and inhibition of the fission regulator Dynamin-related protein 1 (Drp1) reduces proliferation and increases apoptosis of lung cancer cells. Dynasore is a small molecule non-selective inhibitor of the GTPase activity of dynamin 1, dynamin 2, and Drp1 in vivo and in vitro. Here, we investigated the effects of dynasore on the proliferation and apoptosis of A549 lung cancer cells, alone and in combination with the chemotherapeutic drug cisplatin. We found that cisplatin increased mitochondrial fission and dynamin 2 expression, whereas dynasore had the opposite effects. However, both cisplatin and dynasore independently induced mitochondrial oxidative stress, leading to mitochondrial dysfunction, reduced cell proliferation, and enhanced apoptosis. Importantly, dynasore significantly augmented the anti-cancer effects of cisplatin. To the best of our knowledge, this is the first report that dynasore inhibits proliferation and induces apoptosis of lung cancer cells, and enhances the inhibitory effects of cisplatin.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Cisplatino/administração & dosagem
Hidrazonas/administração & dosagem
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/patologia
[Mh] Termos MeSH secundário: Células A549
Antineoplásicos/administração & dosagem
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Seres Humanos
Neoplasias Pulmonares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hydrazones); 0 (N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29232581
[Au] Autor:Rahman FU; Bhatti MZ; Ali A; Duong HQ; Zhang Y; Yang B; Koppireddi S; Lin Y; Wang H; Li ZT; Zhang DW
[Ad] Endereço:Department of Chemistry, Fudan University, 220 Handan Road, Shanghai 200433, China; Department of Materials Science, Fudan University, 220 Handan Road, Shanghai 200433, China.
[Ti] Título:Homo- and heteroleptic Pt(II) complexes of ONN donor hydrazone and 4-picoline: A synthetic, structural and detailed mechanistic anticancer investigation.
[So] Source:Eur J Med Chem;143:1039-1052, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Two series of homoleptic Pt(II)(hydrazone)Cl (C1a-C5a) and heteroleptic Pt(II)(hydrazone)(4-picoline). BF (C1b-C5b) complexes were prepared and characterized by H, C, F NMR and HR ESI-MS. Structure of C2b was confirmed by single crystal X-ray analysis. These complexes were studied for their in vitro anticancer activities in human multiple cancer cells including breast (MCF-7), liver (HepG2), lung (H460), colon (HCT116) and cervical (Hela) cancers. C1a-C5a and C1b-C5b showed considerable anticancer effect. The overall anticancer effect of all these complexes was higher in liver (HepG2) and lung (H460) cancer cell lines and the effect of C2b and C3b was observed to be the highest among these 10 complexes. Therefore, we selected C2b and C3b to study their in vitro anticancer mechanism in HepG2 and H460 cancer cells. C2b and C3b changed cancer cell morphology and inhibited cell migration. The anticancer mechanistic studies demonstrated that C2b and C3b induced cell apoptosis, as evidenced by DAPI and AO/EB staining and flow cytometry analyses. Moreover, qRT-PCR and western blotting analysis showed that H460 and HepG2 cells treated with C2b and C3b significantly increased the expression of p53, p63, p21, p15, Bax and decreased Bcl-2 and c-Myc levels. The DNA binding property of these complexes was investigated by gel electrophoresis using pBR322 plasmid DNA. Taken together, the results obtained from the present study demonstrated the potentials of this new class of Pt(II) complexes in reduction of cell viability, suppression of cell migration and acceleration of apoptosis in different cancer cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Hidrazonas/farmacologia
Compostos Organoplatínicos/farmacologia
Picolinas/farmacologia
Platina/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Hidrazonas/química
Estrutura Molecular
Compostos Organoplatínicos/síntese química
Compostos Organoplatínicos/química
Picolinas/química
Platina/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hydrazones); 0 (Organoplatinum Compounds); 0 (Picolines); 49DFR088MY (Platinum)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


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[PMID]:29120128
[Au] Autor:Mehta RH; Alexander JH; LEVO-CTS Steering Committee Members and Trial Investigators
[Ad] Endereço:Duke Clinical Research Institute, Durham, NC
[Ti] Título:Levosimendan in Cardiac Surgery.
[So] Source:N Engl J Med;377(19):1900-1, 2017 11 09.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hidrazonas
Piridazinas
[Mh] Termos MeSH secundário: Procedimentos Cirúrgicos Cardíacos
Cardiotônicos
Seres Humanos
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Hydrazones); 0 (Pyridazines); 349552KRHK (simendan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171110
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1711938



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