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Pesquisa : D02.455.426.559.389.150 [Categoria DeCS]
Referências encontradas : 1070 [refinar]
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[PMID]:29351887
[Au] Autor:Jin R; Chen Q; Yao S; Bai E; Fu W; Wang L; Wang J; Du X; Wei T; Xu H; Jiang C; Qiu P; Wu J; Li W; Liang G
[Ad] Endereço:Department of Digestive Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; Chemical Biology Research Center, College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Synthesis and anti-tumor activity of EF24 analogues as IKKß inhibitors.
[So] Source:Eur J Med Chem;144:218-228, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:EF24 is an IKKß inhibitor (IC : 72 µM) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKKß were designed and synthesized. Several IKKß inhibitors with better activities than EF24 were screened out and B3 showed best IKKß inhibitory (IC : 6.6 µM). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-κB signal pathway by inhibiting IKKß phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKKß-NF-κB signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKKß inhibitor as anti-tumor precursor.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Compostos de Benzilideno/química
Compostos de Benzilideno/farmacologia
Quinase I-kappa B/antagonistas & inibidores
Piperidonas/química
Piperidonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/uso terapêutico
Linhagem Celular Tumoral
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Quinase I-kappa B/metabolismo
Camundongos Nus
Simulação de Acoplamento Molecular
NF-kappa B/metabolismo
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Fosforilação/efeitos dos fármacos
Piperidonas/síntese química
Piperidonas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (NF-kappa B); 0 (Piperidones); EC 2.7.11.10 (I-kappa B Kinase)
[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:180121
[St] Status:MEDLINE


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[PMID]:29190774
[Au] Autor:Chatterjee PK; Yeboah MM; Solanki MH; Kumar G; Xue X; Pavlov VA; Al-Abed Y; Metz CN
[Ad] Endereço:Center for Biomedical Sciences, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States of America.
[Ti] Título:Activation of the cholinergic anti-inflammatory pathway by GTS-21 attenuates cisplatin-induced acute kidney injury in mice.
[So] Source:PLoS One;12(11):e0188797, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) is the most common side effect of cisplatin, a widely used chemotherapy drug. Although AKI occurs in up to one third of cancer patients receiving cisplatin, effective renal protective strategies are lacking. Cisplatin targets renal proximal tubular epithelial cells leading to inflammation, reactive oxygen species, tubular cell injury, and eventually cell death. The cholinergic anti-inflammatory pathway is a vagus nerve-mediated reflex that suppresses inflammation via α7 nicotinic acetylcholine receptors (α7nAChRs). Our previous studies demonstrated the renoprotective and anti-inflammatory effects of cholinergic agonists, including GTS-21. Therefore, we examined the effect of GTS-21 on cisplatin-induced AKI. Male C57BL/6 mice received either saline or GTS-21 (4mg/kg, i.p.) twice daily for 4 days before cisplatin and treatment continued through euthanasia; 3 days post-cisplatin mice were euthanized and analyzed for markers of renal injury. GTS-21 significantly reduced cisplatin-induced renal dysfunction and injury (p<0.05). GTS-21 significantly attenuated renal Ptgs2/COX-2 mRNA and IL-6, IL-1ß, and CXCL1 protein expression, as well as neutrophil infiltration after cisplatin. GTS-21 blunted cisplatin-induced renal ERK1/2 activation, as well as renal ATP depletion and apoptosis (p<0.05). GTS-21 suppressed the expression of CTR1, a cisplatin influx transporter and enhanced the expression of cisplatin efflux transporters MRP2, MRP4, and MRP6 (p<0.05). Using breast, colon, and lung cancer cell lines we showed that GTS-21 did not inhibit cisplatin's tumor cell killing activity. GTS-21 protects against cisplatin-AKI by attenuating renal inflammation, ATP depletion and apoptosis, as well as by decreasing renal cisplatin influx and increasing efflux, without impairing cisplatin-mediated tumor cell killing. Our results support further exploring the cholinergic anti-inflammatory pathway for preventing cisplatin-induced AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Compostos de Benzilideno/farmacologia
Cisplatino/efeitos adversos
Inflamação/prevenção & controle
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylidene Compounds); 0 (Pyridines); 8S399XDN2K (3-(2,4-dimethoxybenzylidene)anabaseine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188797


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[PMID]:29115894
[Au] Autor:Pessôa MTC; Alves SLG; Taranto AG; Villar JAFP; Blanco G; Barbosa LA
[Ad] Endereço:a Laboratório de Bioquímica Celular , Universidade Federal de São João del Rei, Campus Centro-Oeste Dona Lindú , Divinópolis , Brazil.
[Ti] Título:Selectivity analyses of γ-benzylidene digoxin derivatives to different Na,K-ATPase α isoforms: a molecular docking approach.
[So] Source:J Enzyme Inhib Med Chem;33(1):85-97, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Digoxin and other cardiotonic steroids (CTS) exert their effect by inhibiting Na,K-ATPase (NKA) activity. CTS bind to the various NKA isoforms that are expressed in different cell types, which gives CTS their narrow therapeutic index. We have synthesised a series of digoxin derivatives (γ-Benzylidene digoxin derivatives) with substitutions in the lactone ring (including non-oxygen and ether groups), to obtain CTS with better NKA isoform specificity. Some of these derivatives show some NKA isoform selective effects, with BD-3, BD-8, and BD-13 increasing NKA α2 activity, BD-5 inhibiting NKA α1 and NKA α3, BD-10 reducing NKA α1, but stimulating NKA α2 and α3; and BD-14, BD-15, and BD-16 enhancing NKA α3 activity. A molecular-docking approach favoured NKA isoform specific interactions for the compounds that supported their observed activity. These results show that BD compounds are a new type of CTS with the capacity to target NKA activity in an isoform-specific manner.
[Mh] Termos MeSH primário: Compostos de Benzilideno/farmacologia
Digoxina/farmacologia
Simulação de Acoplamento Molecular
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/química
Células Cultivadas
Digoxina/síntese química
Digoxina/química
Relação Dose-Resposta a Droga
Isoenzimas/antagonistas & inibidores
Isoenzimas/metabolismo
Conformação Molecular
Células Sf9
ATPase Trocadora de Sódio-Potássio/metabolismo
Spodoptera
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylidene Compounds); 0 (Isoenzymes); 73K4184T59 (Digoxin); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[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:171109
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1380637


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[PMID]:29023592
[Au] Autor:Niu Z; Pang RTK; Liu W; Li Q; Cheng R; Yeung WSB
[Ad] Endereço:Department of Obstetrics and Gynecology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
[Ti] Título:Polymer-based precipitation preserves biological activities of extracellular vesicles from an endometrial cell line.
[So] Source:PLoS One;12(10):e0186534, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extracellular vesicles (EVs) are membrane-bound vesicles released by cells and act as media for transfer of proteins, small RNAs and mRNAs to distant sites. They can be isolated by different methods. However, the biological activities of the purified EVs have seldom been studied. In this study, we compared the use of ultracentrifugation (UC), ultra-filtration (UF), polymer-based precipitation (PBP), and PBP with size-based purification (PBP+SP) for isolation of EVs from human endometrial cells and mouse uterine luminal fluid (ULF). Electron microscopy revealed that the diameters of the isolated EVs were similar among the tested methods. UF recovered the highest number of EVs followed by PBP, while UC and PBP+SP were significantly less efficient (P<0.05). Based on the number of EVs-to-protein ratios, PBP had the least protein contamination, significantly better than the other methods (P<0.05). All the isolated EVs expressed exosome-enriched proteins CD63, TSG101 and HSP70. Incubation of the trophoblast JEG-3 cells with an equal amount of the fluorescence-labelled EVs isolated by the studied methods showed that many of the PBP-EVs treated cells were fluorescence positive but only a few cells were labelled in the UC- and UF-EVs treated groups. Moreover, the PBP-EVs could transfer significantly more miRNA to the recipient cells than the other 3 methods (P<0.05). The PBP method could isolate EVs from mouse ULF; the diameter of the isolated EVs was 62±19 nm and expressed CD63, TSG101 and HSP70 proteins. In conclusion, PBP could best preserve the activities of the isolated EVs among the 4 methods studied and was able to isolate EVs from a small volume of sample. The simple setup and low equipment demands makes PBP the most suitable method for rapid EV assessment and isolation of EVs in clinical and basic research settings.
[Mh] Termos MeSH primário: Vesículas Extracelulares/metabolismo
Polímeros/química
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Compostos de Benzilideno/farmacologia
Blastocisto/citologia
Blastocisto/metabolismo
Linhagem Celular
Precipitação Química
Técnicas de Cocultura
Proteínas de Ligação a DNA/metabolismo
Neoplasias do Endométrio/metabolismo
Neoplasias do Endométrio/patologia
Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Exossomos/efeitos dos fármacos
Exossomos/metabolismo
Vesículas Extracelulares/ultraestrutura
Feminino
Proteínas de Choque Térmico HSP70/metabolismo
Seres Humanos
Camundongos
MicroRNAs/metabolismo
Microscopia Eletrônica
Microscopia de Fluorescência
Tetraspanina 30/metabolismo
Fatores de Transcrição/metabolismo
Trofoblastos/citologia
Trofoblastos/metabolismo
Ultracentrifugação
Ultrafiltração
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Benzylidene Compounds); 0 (DNA-Binding Proteins); 0 (Endosomal Sorting Complexes Required for Transport); 0 (GW 4869); 0 (HSP70 Heat-Shock Proteins); 0 (MicroRNAs); 0 (Polymers); 0 (Tetraspanin 30); 0 (Transcription Factors); 0 (Tsg101 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186534


  5 / 1070 MEDLINE  
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[PMID]:28982855
[Au] Autor:Bakalova R; Zhelev Z; Shibata S; Nikolova B; Aoki I; Higashi T
[Ad] Endereço:Department of Molecular Imaging and Theranostics, National Institute of Radiological Sciences (NIRS), National Institute for Quantum and Radiological Science and Technology (QST), Chiba, Japan bakalova.rumiana@qst.go.jp.
[Ti] Título:Impressive Suppression of Colon Cancer Growth by Triple Combination SN38/EF24/Melatonin: "Oncogenic" "Onco-Suppressive" Reactive Oxygen Species.
[So] Source:Anticancer Res;37(10):5449-5458, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The study aimed to investigate the effect of multi-targeted combinations (SN38/EF24; SN38/EF24/melatonin) on the growth of colon cancer in experimental animals and their impact on the ratio "oncogenic"/"onco-suppressive" reactive oxygen species (ROS) - a crucial factor for triggering carcinogenesis, as well as for development of effective therapeutic strategies. MATERIALS AND METHODS: The experiments were conducted on colon cancer-grafted mice - non-treated, SN38/EF24-treated and SN38/EF24/melatonin-treated within 22 days. The balance between different types of ROS was measured in vivo by nitroxide-enhanced magnetic resonance imaging (MRI), as well as on isolated tissue specimens by conventional analytical tests. RESULTS: Both combinations significantly suppressed the tumor growth. Impressive anticancer effect was observed in SN38/EF24/melatonin-treated mice - almost complete destruction of the tumor. Both types of ROS (superoxide and hydroperoxides) were elevated in cancer, but the MRI data suggest that the ratio between them tends towards superoxide. SN38/EF24 decreased the level of superoxide, but did not affect the level of hydroperoxides in the cancerous tissue, while SN38/EF24/melatonin decreased the level of superoxide below the control and increased significantly the level of hydroperoxides. CONCLUSION: The most important observations are that: (i) colon cancer was characterized by a vicious cycle, that ensures a permanent domination of "oncogenic" ROS (as superoxide) over "onco-suppressive" ROS (as hydrogen peroxide); (ii) the anticancer effect of the triple combination EF24/SN38/melatonin was accompanied by decreasing "oncogenic" and increasing "onco-suppressive" ROS; (iii) the ratio between both types of ROS could be a new onco-target for combined therapy; and (iv) nitroxide-enhanced MRI is a valuable tool for analyzing of this ratio.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Compostos de Benzilideno/farmacologia
Camptotecina/análogos & derivados
Proliferação Celular/efeitos dos fármacos
Neoplasias Colorretais/tratamento farmacológico
Melatonina/farmacologia
Oncogenes
Estresse Oxidativo/efeitos dos fármacos
Piperidonas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Camptotecina/farmacologia
Linhagem Celular Tumoral
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Peróxido de Hidrogênio/metabolismo
Imagem por Ressonância Magnética
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Transdução de Sinais/efeitos dos fármacos
Superóxidos/metabolismo
Fatores de Tempo
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Benzylidene Compounds); 0 (Piperidones); 0 (Reactive Oxygen Species); 11062-77-4 (Superoxides); 7673326042 (irinotecan); BBX060AN9V (Hydrogen Peroxide); JL5DK93RCL (Melatonin); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  6 / 1070 MEDLINE  
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[PMID]:28934264
[Au] Autor:Asahi H; Inoue SI; Niikura M; Kunigo K; Suzuki Y; Kobayashi F; Sendo F
[Ad] Endereço:Department of Infectious Diseases, Division of Tropical Diseases and Parasitology, Kyorin University School of Medicine, Tokyo, Japan.
[Ti] Título:Profiling molecular factors associated with pyknosis and developmental arrest induced by an opioid receptor antagonist and dihydroartemisinin in Plasmodium falciparum.
[So] Source:PLoS One;12(9):e0184874, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malaria continues to be a devastating disease, largely caused by Plasmodium falciparum infection. We investigated the effects of opioid and cannabinoid receptor antagonists on the growth of intraerythrocytic P. falciparum. The delta opioid receptor antagonist 7-benzylidenenaltrexone (BNTX) and the cannabinoid receptor antagonists rimonaband and SR144528 caused growth arrest of the parasite. Notably BNTX and the established antimalarial drug dihydroartemisinin induced prominent pyknosis in parasite cells after a short period of incubation. We compared genome-wide transcriptome profiles in P. falciparum with different degrees of pyknosis in response to drug treatment, and identified 11 transcripts potentially associated with the evoking of pyknosis, of which three, including glutathione reductase (PfGR), triose phosphate transporter (PfoTPT), and a conserved Plasmodium membrane protein, showed markedly different gene expression levels in accordance with the degree of pyknosis. Furthermore, the use of specific inhibitors confirmed PfGR but not PfoTPT as a possible factor contributing to the development of pyknosis. A reduction in total glutathione levels was also detected in association with increased pyknosis. These results further our understanding of the mechanisms responsible for P. falciparum development and the antimalarial activity of dihydroartemisinin, and provide useful information for the development of novel antimalarial agents.
[Mh] Termos MeSH primário: Antimaláricos/farmacologia
Artemisininas/farmacologia
Antagonistas de Receptores de Canabinoides/farmacologia
Antagonistas de Entorpecentes/farmacologia
Plasmodium falciparum/efeitos dos fármacos
Plasmodium falciparum/metabolismo
[Mh] Termos MeSH secundário: Compostos de Benzilideno/farmacologia
Bornanos/farmacologia
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
Cromatina/efeitos dos fármacos
Cromatina/metabolismo
Relação Dose-Resposta a Droga
Perfilação da Expressão Gênica
Glutationa/metabolismo
Naltrexona/análogos & derivados
Naltrexona/farmacologia
Oxirredução
Piperidinas/farmacologia
Plasmodium falciparum/crescimento & desenvolvimento
Pirazóis/farmacologia
Transcriptoma/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Artemisinins); 0 (Benzylidene Compounds); 0 (Bornanes); 0 (Cannabinoid Receptor Antagonists); 0 (Chromatin); 0 (Narcotic Antagonists); 0 (Piperidines); 0 (Pyrazoles); 0 (SR 144528); 129468-28-6 (7-benzylidenenaltrexone); 5S6W795CQM (Naltrexone); 6A9O50735X (dihydroartemisinin); GAN16C9B8O (Glutathione); RML78EN3XE (rimonabant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184874


  7 / 1070 MEDLINE  
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[PMID]:28791708
[Au] Autor:Cao YL; Zhuang T; Xing BH; Li N; Li Q
[Ad] Endereço:Department of Gynaecology and Obstetrics, Cangzhou Center Hospital, Cangzhou, China.
[Ti] Título:Exosomal DNMT1 mediates cisplatin resistance in ovarian cancer.
[So] Source:Cell Biochem Funct;35(6):296-303, 2017 Aug.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ovarian cancer is the most common malignancy in women. Owing to late syndromic presentation and lack of efficient early detection, most cases are diagnosed at advanced stages. Surgery and platinum-based chemotherapy are still the standard care currently. However, resistance invoked often compromises the clinical value of the latter. Expression of DNA methyltransferase 1 (DNMT1) was analysed by gene array. Protein was determined by immunoblotting. Exosome was isolated with commercial kit. Cell proliferation was measured by CCK8 method. Annexin V-PI double staining was performed for apoptosis evaluation. Xenograft model was established and administrated with exosome. Tumour growth and overall survival were monitored. We demonstrated the upregulation of DNMT1 in both tumour and derived cell line. DNMT1 transcripts were highly enriched in exosomes from conditioned medium of ovarian cells. Co-incubation with exosomes stimulated endogenous expression and rendered host cell the resistance to cytotoxicity of cisplatin. In vivo administration of DNMT1-containing exosomes exacerbated xenograft progression and reduced overall survival significantly. Moreover, treatment with exosome inhibitor GW4869 almost completely restored sensitivity in resistant cells. Our data elucidated an unappreciated mechanism of exosomal DNMT1 in cisplatin resistance in ovarian cancer, also indicating the potential of the combination of exosome inhibitor with cisplatin in resistant patients.
[Mh] Termos MeSH primário: Cisplatino/uso terapêutico
DNA (Citosina-5-)-Metiltransferases/metabolismo
Exossomos/enzimologia
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Compostos de Benzilideno/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Cisplatino/toxicidade
DNA (Citosina-5-)-Metiltransferase 1
DNA (Citosina-5-)-Metiltransferases/genética
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
RNA Mensageiro/metabolismo
Transplante Heterólogo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (GW 4869); 0 (RNA, Messenger); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNMT1 protein, human); EC 2.1.1.37 (Dnmt1 protein, mouse); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3276


  8 / 1070 MEDLINE  
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[PMID]:28668885
[Au] Autor:Ohkura K; Tatematsu Y; Kawaguchi Y; Uto Y; Hori H
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Suzuka University of Medical Science Graduate School, Suzuka, Japan kohkura@suzuka-u.ac.jp.
[Ti] Título:Interactive Analysis of TX-1123 with Cyclo-oxygenase: Design of COX2 Selective TX Analogs.
[So] Source:Anticancer Res;37(7):3849-3854, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To date, two cyclo-oxygenase (COX) isoforms, COX1 and COX2, have been identified. In the present study, the COX-inhibitory activities of TX-1123 derivatives with the 2-hydroxyarylidene-4-cyclopentene-1,3-dione structure were examined, and the binding profiles of TX-1123 to COXs were analyzed using docking simulations. MATERIALS AND METHODS: X-Ray data on COX1 [protein data bank (PDB) ID=1PGG] and COX2 (PDB ID=3LN1) were used for molecular interactive simulations. The interactive profiles of TX-1123 derivatives with COXs were examined using a molecular simulation technique with Molegro Virtual Docker (CLC bio, Aarhus, Denmark). RESULTS: TX-1123 exhibited COX1-inhibitory activity [half-maximal-inhibitory concentration (IC )=1.57×10 M]. The COX2 inhibitory activity of TX-1123 was potent (IC =1.16×10 M), and the ratio of COX1/COX2 inhibition was 13.5. TX-1123 bound to the COX2 molecule, and the oxygen atom of the 4-cyclopentene-1,3-dione region of TX-1123 interacted with Cys and Gln of COX2. CONCLUSION: The TX-1123-binding pocket of COX2 differs from that of the COX2-selective celecoxib-binding pocket. TX-1123 exhibited a different COX2-interactive mechanism from that of celecoxib.
[Mh] Termos MeSH primário: Compostos de Benzilideno/farmacologia
Ciclo-Oxigenase 1/metabolismo
Ciclo-Oxigenase 2/metabolismo
Ciclopentanos/farmacologia
[Mh] Termos MeSH secundário: Sítios de Ligação
Celecoxib/farmacologia
Ciclo-Oxigenase 1/química
Ciclo-Oxigenase 2/química
Cisteína/metabolismo
Glutamina/metabolismo
Seres Humanos
Modelos Moleculares
Simulação de Acoplamento Molecular
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxyarylidene-4-cyclopentene-1,3-dione); 0 (Benzylidene Compounds); 0 (Cyclopentanes); 0RH81L854J (Glutamine); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS1 protein, human); EC 1.14.99.1 (PTGS2 protein, human); JCX84Q7J1L (Celecoxib); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


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[PMID]:28667694
[Au] Autor:Matsumoto A; Takahashi Y; Nishikawa M; Sano K; Morishita M; Charoenviriyakul C; Saji H; Takakura Y
[Ad] Endereço:Department of Biopharmaceutics and Drug Metabolism, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, Japan.
[Ti] Título:Accelerated growth of B16BL6 tumor in mice through efficient uptake of their own exosomes by B16BL6 cells.
[So] Source:Cancer Sci;108(9):1803-1810, 2017 Sep.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Exosomes are extracellular vesicles released by various cell types and play roles in cell-cell communication. Several studies indicate that cancer cell-derived exosomes play important pathophysiological roles in tumor progression. Biodistribution of cancer cell-derived exosomes in tumor tissue is an important factor for determining their role in tumor proliferation; however, limited studies have assessed the biodistribution of exosomes in tumor tissues. In the present study, we examined the effect of cancer-cell derived exosomes on tumor growth by analyzing their biodistribution. Murine melanoma B16BL6-derived exosomes increased the proliferation and inhibited the apoptosis of B16BL6 cells, which was associated with an increase and decrease in the levels of proliferation- and apoptosis-related proteins, respectively. GW4869-induced inhibition of exosome secretion decreased the proliferation of B16BL6 cells, and treatment of GW4869-treated cells with B16BL6-derived exosomes restored their proliferation. Next, we treated B16BL6 tumors in mice with B16BL6-derived exosomes and examined the biodistribution and cellular uptake of these exosomes. After the intratumoral injection of radiolabeled B16BL6-derived exosomes, most radioactivity was detected within the tumor tissues of mice. Fractionation of cells present in the tumor tissue showed that fluorescently labeled exosomes were mainly taken up by B16BL6 cells. Moreover, intratumoral injection of B16BL6-derived exosomes promoted tumor growth, whereas intratumoral injection of GW4869 suppressed tumor growth. These results indicate that B16BL6 cells secrete and take up their own exosomes to induce their proliferation and inhibit their apoptosis, which promotes tumor progression.
[Mh] Termos MeSH primário: Exossomos/metabolismo
Melanoma Experimental/patologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Antineoplásicos/farmacologia
Apoptose
Proteínas Reguladoras de Apoptose/metabolismo
Compostos de Benzilideno/farmacologia
Linhagem Celular Tumoral
Proliferação Celular
Ensaios de Seleção de Medicamentos Antitumorais
Exossomos/secreção
Masculino
Melanoma Experimental/metabolismo
Camundongos Endogâmicos C57BL
Transplante de Neoplasias
Neoplasias Cutâneas/metabolismo
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (Benzylidene Compounds); 0 (GW 4869)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13310


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[PMID]:28662966
[Au] Autor:Kutsumura N; Koyama Y; Nagumo Y; Nakajima R; Miyata Y; Yamamoto N; Saitoh T; Yoshida N; Iwata S; Nagase H
[Ad] Endereço:International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
[Ti] Título:Antitrichomonal activity of δ opioid receptor antagonists, 7-benzylidenenaltrexone derivatives.
[So] Source:Bioorg Med Chem;25(16):4375-4383, 2017 Aug 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The 7-benzylidenenaltrexone (BNTX) derivatives 2a-v, 3a-c, 13a-c, and 14a were synthesized from naltrexone (1) and evaluated for their antitrichomonal activity. The structure-activity-relationship studies found that 4-iodo-BNTX (2g) showed the highest activity (IC =10.5µM) and the affinity for the opioid receptor was less important for antitrichomonal activity against Trichomonas vaginalis. The morphinan skeleton bearing both the double bond for a Michael acceptor and the phenolic hydroxy group would be a specific template for development of antitrichomonal agents. In addition, the mechanism of the antitrichomonal activity of the BNTX derivatives may differ from that of the standard drug, metronidazole.
[Mh] Termos MeSH primário: Antitricômonas/farmacologia
Compostos de Benzilideno/farmacologia
Naltrexona/análogos & derivados
Receptores Opioides delta/antagonistas & inibidores
Trichomonas vaginalis/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antitricômonas/síntese química
Antitricômonas/química
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/química
Células CHO
Cricetulus
Relação Dose-Resposta a Droga
Estrutura Molecular
Naltrexona/síntese química
Naltrexona/química
Naltrexona/farmacologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antitrichomonal Agents); 0 (Benzylidene Compounds); 0 (Receptors, Opioid, delta); 129468-28-6 (7-benzylidenenaltrexone); 5S6W795CQM (Naltrexone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE



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