Base de dados : MEDLINE
Pesquisa : D02.500.375 [Categoria DeCS]
Referências encontradas : 3523 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 353 ir para página                         

  1 / 3523 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29331658
[Au] Autor:Chatterjee S; Rhee Y; Chung PS; Ge RF; Ahn JC
[Ad] Endereço:Beckman Laser Institute Korea, Dankook University, Cheonan 31116, Republic of Korea.
[Ti] Título:Sulforaphene Enhances The Efficacy of Photodynamic Therapy In Anaplastic Thyroid Cancer Through Ras/RAF/MEK/ERK Pathway Suppression.
[So] Source:J Photochem Photobiol B;179:46-53, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Sulforaphene (SFE), a natural isothiocyanate from cruciferous vegetables has shown a potential anticancer effect against cervical and lung cancer. Palliative treatments like photodynamic therapy (PDT) are being implemented for a long time however, the results are still not promising in case of aggressive cancers like anaplastic thyroid cancer. The objective of this work is to establish an alternative method with the combination of photofrin-PDT and sulforaphene, a natural isothiocyanate from cruciferous vegetables, against human anaplastic thyroid cancer to enhance the efficacy of PDT. In this study, cell viability of FRO cells due to combination treatment was analyzed by MTT assay, Cell cycle arrest, MMP depolarization and ROS generation, analyzed by flow cytometry. Western blot analysis of various proliferative proteins was performed to assess the activity of combination treatment against FRO cells. From the results, sulforaphene alone showed no cytotoxicity against normal cells, however, combination of sulforaphene and photofrin mediated PDT showed a noticeable decrease in cell proliferation against FRO cells. Combination treatment synergistically caused cell cycle arrest via ROS generation and MMP depolarization. The expressions of Ras, MEK, ERK, B-Raf proteins significantly modulated due to combination treatment. PDT and SFE can induce apoptosis in anaplastic thyroid cancer cells individually but while treated in combination, it enhanced the apoptotic and anti-proliferative effect, much higher than the individual doses. In summary, our work designates sulforaphene as a unique natural enhancer of efficacy with PDT against anaplastic thyroid cancer.
[Mh] Termos MeSH primário: MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Isotiocianatos/farmacologia
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Fármacos Fotossensibilizantes/farmacologia
Transdução de Sinais/efeitos dos fármacos
Quinases raf/metabolismo
Proteínas ras/metabolismo
[Mh] Termos MeSH secundário: Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Éter de Diematoporfirina/farmacologia
Éter de Diematoporfirina/uso terapêutico
MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores
Seres Humanos
Isotiocianatos/uso terapêutico
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Fotoquimioterapia
Fármacos Fotossensibilizantes/uso terapêutico
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Espécies Reativas de Oxigênio/metabolismo
Carcinoma Anaplásico da Tireoide/tratamento farmacológico
Carcinoma Anaplásico da Tireoide/metabolismo
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/tratamento farmacológico
Neoplasias da Glândula Tireoide/metabolismo
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isothiocyanates); 0 (Photosensitizing Agents); 0 (Protein Kinase Inhibitors); 0 (Reactive Oxygen Species); 0 (sulphoraphene); 97067-70-4 (Dihematoporphyrin Ether); EC 2.7.11.1 (raf Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


  2 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29314795
[Au] Autor:Konic-Ristic A; Stanojkovic T; Srdic-Rajic T; Dilber S; Dordevic B; Stankovic I; Juranic Z
[Ti] Título:In vitro assessment of antiproliferative action selectivity of dietary isothiocyanates for tumor versus normal human cells.
[So] Source:Vojnosanit Pregl;73(7):636-42, 2016 Jul.
[Is] ISSN:0042-8450
[Cp] País de publicação:Serbia
[La] Idioma:eng
[Ab] Resumo:Background/Aim: Numerous epidemiological studies have shown beneficial effects of cruciferous vegetables consumption in cancer chemoprevention. Biologically active compounds of different Brassicaceae species with antitumor potential are isothiocyanates, present in the form of their precursors - glucosinolates. The aim of this study was to determine the selectivity of antiproliferative action of dietary isothiocyanates for malignant versus normal cells. Methods: Antiproliferative activity of three isothiocyanates abundant in human diet: sulforaphane, benzyl isothiocyanate (BITC) and phenylethyl isothiocyanate, on human cervix carcinoma cell line - HeLa, melanoma cell line - Fem-x, and colon cancer cell line - LS 174, and on peripheral blood mononuclear cells (PBMC), with or without mitogen, were determined by MTT colorimetric assay 72 h after their continuous action. Results: All investigated isothiocyanates inhibited the proliferation of HeLa, Fem-x and LS 174 cells. On all cell lines treated, BITC was the most potent inhibitor of cell proliferation with half-maximum inhibitory concentration (IC50) values of 5.04 mmoL m-3 on HeLa cells, 2.76 mmol m-3 on Fem-x, and 14.30 mmol m-3 on LS 174 cells. Antiproliferative effects on human PBMC were with higher IC50 than on malignant cells. Indexes of selectivity, calculated as a ratio between IC50 values obtained on PBMC and malignant cells, were between 1.12 and 16.57, with the highest values obtained for the action of BITC on melanoma Fem-x cells. Conclusion: Based on its antiproliferative effects on malignant cells, as well as the selectivity of the action to malignant vs normal cells, benzyl isothiocyanate can be considered as a promising candidate in cancer chemoprevention. In general, the safety of investigated compounds, in addition to their antitumor potential, should be considered as an important criterion in cancer chemoprevention. Screening of selectivity is a plausible approach to the evaluation of safety of both natural isothiocyanates and synthesised analogues of these bioactive compounds.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Proliferação Celular/efeitos dos fármacos
Dieta
Isotiocianatos/farmacologia
Neoplasias/prevenção & controle
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Células HeLa
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Neoplasias/patologia
Células Tumorais Cultivadas
Verduras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Isothiocyanates)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.2298/VSP141103066K


  3 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29307179
[Au] Autor:Morroni F; Sita G; Djemil A; D'Amico M; Pruccoli L; Cantelli-Forti G; Hrelia P; Tarozzi A
[Ad] Endereço:Department of Pharmacy and Biotechnology, Alma Mater Studiorum-University of Bologna , Bologna, Italy.
[Ti] Título:Comparison of Adaptive Neuroprotective Mechanisms of Sulforaphane and its Interconversion Product Erucin in in Vitro and in Vivo Models of Parkinson's Disease.
[So] Source:J Agric Food Chem;66(4):856-865, 2018 Jan 31.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several studies suggest that an increase of glutathione (GSH) through activation of the transcriptional nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in the dopaminergic neurons may be a promising neuroprotective strategy in Parkinson's disease (PD). Among Nrf2 activators, isothiocyanate sulforaphane (SFN), derived from precursor glucosinolate present in Brassica vegetables, has gained attention as a potential neuroprotective compound. Bioavailability studies also suggest the contribution of SFN metabolites, including erucin (ERN), to the neuroprotective effects of SFN. Therefore, we compared the in vitro neuroprotective effects of SFN and ERN at the same dose level (5 µM) and oxidative treatment with 6-hydroxydopamine (6-OHDA) in SH-SY5Y cells. The pretreatment of SH-SY5Y cells with SFN recorded a higher (p < 0.05) active nuclear Nrf2 protein (12.0 ± 0.4 vs 8.0 ± 0.2 fold increase), mRNA Nrf2 (2.0 ± 0.3 vs 1.4 ± 0.1 fold increase), total GSH (384.0 ± 9.0 vs 256.0 ± 8.0 µM) levels, and resistance to neuronal apoptosis elicited by 6-OHDA compared to ERN. By contrast, the simultaneous treatment of SH-SY5Y cells with either SFN or ERN and 6-OHDA recorded similar neuroprotective effects with both the isothiocyanates (Nrf2 protein 2.2 ± 0.2 vs 2.1 ± 0.1 and mRNA Nrf2 2.1 ± 0.3 vs 1.9 ± 0.2 fold increase; total GSH 384.0 ± 4.8 vs 352.0 ± 6.4 µM). Finally, in vitro finding was confirmed in a 6-OHDA-PD mouse model. The metabolic oxidation of ERN to SFN could account for their similar neuroprotective effects in vivo, raising the possibility of using vegetables containing a precursor of ERN for systemic antioxidant benefits in a similar manner to SFN.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/efeitos dos fármacos
Isotiocianatos/farmacologia
Fármacos Neuroprotetores/farmacologia
Doença de Parkinson/prevenção & controle
Sulfetos/farmacologia
Tiocianatos/farmacologia
[Mh] Termos MeSH secundário: Animais
Brassica/química
Linhagem Celular Tumoral
Neurônios Dopaminérgicos/química
Glutationa/análise
Seres Humanos
Isotiocianatos/metabolismo
Isotiocianatos/uso terapêutico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fator 2 Relacionado a NF-E2/análise
Fator 2 Relacionado a NF-E2/genética
Neuroblastoma
Fármacos Neuroprotetores/uso terapêutico
Oxirredução
Oxidopamina/administração & dosagem
RNA Mensageiro/análise
Sulfetos/metabolismo
Sulfetos/uso terapêutico
Tiocianatos/metabolismo
Tiocianatos/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isothiocyanates); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Neuroprotective Agents); 0 (RNA, Messenger); 0 (Sulfides); 0 (Thiocyanates); 8HW4YBZ748 (Oxidopamine); CTE370DL3U (erucin); GA49J4310U (sulforafan); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04641


  4 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29247643
[Au] Autor:Wang H; Wang F; Wu S; Liu Z; Li T; Mao L; Zhang J; Li C; Liu C; Yang Y
[Ad] Endereço:Center for Molecular Medicine (CMM), School of Life Science and Biotechnology, Dalian University of Technology, Dalian 116023, China.
[Ti] Título:Traditional herbal medicine-derived sulforaphene promotes mitophagic cell death in lymphoma cells through CRM1-mediated p62/SQSTM1 accumulation and AMPK activation.
[So] Source:Chem Biol Interact;281:11-23, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Sulforaphene (LFS-01) is the major chemical constituent of Raphanus sativus, a medicinal herb used for over a thousand years in traditional Chinese medicine. Here we identified that LFS-01 can selectively eradicate lymphoma cells while sparing normal lymphocytes by triggering concomitant mitophagy and apoptosis. We demonstrated that LFS-01 can retain Nrf2 in the nucleus by covalently modulating CRM1 and consequently upregulate p62/SQSTM1, an essential structural component of the autophagosomes during mitophagic process. We found that LFS-01 treatment also stimulated AMPK and thereby inhibited the mTOR pathway. On the contrary, we revealed that AMPK inhibition can severely impair the LFS-01-mediated mitophagy. Transcriptomic studies confirmed that 15 autophagy-associated genes such as p62/SQSTM1, VCP and BCL2 were differentially expressed after LFS-01 treatment. Furthermore, protein interactome network analysis revealed that the events of apoptosis and the assembly of autophagy vacuole were significant upon LFS-01 exposure. Lastly, we found that LFS-01 exhibited strong efficacy in xenograft mouse model yet with the lack of apparent toxicity to animals. We concluded that LFS-01 triggered mitophagic cell death via CRM1-mediated p62 overexpression and AMPK activation. Our findings provide new insights into the mechanism of action for LFS-01 and highlight its potential applications in treating major human diseases.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Apoptose/efeitos dos fármacos
Medicamentos de Ervas Chinesas/química
Isotiocianatos/farmacologia
Carioferinas/metabolismo
Degradação Mitocondrial/efeitos dos fármacos
Receptores Citoplasmáticos e Nucleares/metabolismo
Proteína Sequestossoma-1/metabolismo
[Mh] Termos MeSH secundário: Animais
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Seres Humanos
Isotiocianatos/química
Isotiocianatos/uso terapêutico
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/metabolismo
Linfoma/tratamento farmacológico
Linfoma/metabolismo
Linfoma/patologia
Camundongos
Camundongos Endogâmicos BALB C
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Estrutura Terciária de Proteína
Raphanus/química
Raphanus/metabolismo
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Isothiocyanates); 0 (Karyopherins); 0 (Receptors, Cytoplasmic and Nuclear); 0 (SQSTM1 protein, human); 0 (Sequestosome-1 Protein); 0 (exportin 1 protein); 0 (sulphoraphene); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[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:171217
[St] Status:MEDLINE


  5 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28449614
[Au] Autor:Encinas-Basurto D; Ibarra J; Juarez J; Burboa MG; Barbosa S; Taboada P; Troncoso-Rojas R; Valdez MA
[Ad] Endereço:a Departamento de Física , Posgrado en Nanotecnología, Universidad de Sonora, Rosales y Transversal , Hermosillo , Sonora , México.
[Ti] Título:Poly(lactic-co-glycolic acid) nanoparticles for sustained release of allyl isothiocyanate: characterization, in vitro release and biological activity.
[So] Source:J Microencapsul;34(3):231-242, 2017 May.
[Is] ISSN:1464-5246
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objective of this study is to establish the ability of entrap allyl isothiocyanate (AITC) into polymeric nanoparticles to extend its shelf life and enhance its antiproliferative properties. Natural compounds, such as AITC, have showed multi-targeting activity resulting in a wide-range spectrum of therapeutic properties in chronic and degenerative diseases, conversely with most current pharmaceutical drugs showing single targeting activity and often result in drug resistance after extended administration periods. Apparently, AITC-loaded poly(lactic-co-glycolic acid) nanoparticles (PLGA NPs) reduced AITC degradation and volatility and were able to extend AITC shelf life compared with free AITC (65% vs. 20% in 24 h, respectively). Cell viability and uptake of AITC-loaded nanoparticles were studied in vitro, showing that the protection and sustained release of AITC from polymeric NPs involved a larger toxicity of tumoral cells. These nanoparticles could be used as protective systems for enhancing a biological activity.
[Mh] Termos MeSH primário: Preparações de Ação Retardada
Portadores de Fármacos/química
Isotiocianatos/administração & dosagem
Ácido Láctico/química
Nanopartículas/química
Ácido Poliglicólico/química
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Delayed-Action Preparations); 0 (Drug Carriers); 0 (Isothiocyanates); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); BN34FX42G3 (allyl isothiocyanate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1080/02652048.2017.1323037


  6 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27774770
[Au] Autor:Chen C; Jiang X; Gu S; Lai Y; Liu Y; Zhang Z
[Ad] Endereço:Department of Occupational and Environmental Health, West China School of Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
[Ti] Título:Protection of Nrf2 against arsenite-induced oxidative damage is regulated by the cyclic guanosine monophosphate-protein kinase G signaling pathway.
[So] Source:Environ Toxicol;32(8):2004-2020, 2017 Aug.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arsenite has been shown to induce a variety of oxidative damage in mammalian cells. However, the mechanisms underlying cellular responses to its adverse effects remain unknown. We previously showed that the level of Nrf2, a nuclear transcription factor significantly increased in arsenite-treated human bronchial epithelial (HBE) cells suggesting that Nrf2 is involved in responding to arsenite-induced oxidative damage. To explore how Nrf2 can impact arsenite-induced oxidative damage, in this study, we examined Nrf2 activation and its regulation upon cellular arsenite exposure as well as its effects on arsenite-induced oxidative damage in HBE cells. We found that Nrf2 mRNA and protein levels were significantly increased by arsenite in a dose- and time-dependent manner. Furthermore, we showed that over-expression of Nrf2 significantly reduced the level of arsenite-induced oxidative damage in HBE cells including DNA damage, chromosomal breakage, lipid peroxidation and depletion of antioxidants. This indicates a protective role of Nrf2 against arsenite toxicity. This was further supported by the fact that activation of Nrf2 by its agonists, tertiary butylhydroquinone (t-BHQ) and sulforaphane (SFN) resulted in the same protective effects against arsenite toxicity. Moreover, we demonstrated that arsenite-induced activation of Nrf2 was mediated by the cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signaling pathway. This is the first evidence showing that Nrf2 protects against arsenite-induced oxidative damage through the cGMP-PKG pathway. Our study suggests that activation of Nrf2 through the cGMP-PKG signaling pathway in HBE cells may be developed as a new strategy for prevention of arsenite toxicity. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2004-2020, 2017.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Proteínas Quinases Dependentes de GMP Cíclico/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Linhagem Celular
Seres Humanos
Hidroquinonas/farmacologia
Isotiocianatos/farmacologia
Fator 2 Relacionado a NF-E2/agonistas
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Arsenites); 0 (Hydroquinones); 0 (Isothiocyanates); 0 (NF-E2-Related Factor 2); C12674942B (2-tert-butylhydroquinone); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases); GA49J4310U (sulforafan); N5509X556J (arsenite)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22374


  7 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28873563
[Au] Autor:Jastrzebska A; Piasta A; Krzeminski M; Szlyk E
[Ad] Endereço:Faculty of Chemistry, Nicolaus Copernicus University in Torun, Gagarin 7 Str., 87-100 Torun, Poland. Electronic address: aj@chem.uni.torun.pl.
[Ti] Título:Application of 3,5-bis-(trifluoromethyl)phenyl isothiocyanate for the determination of selected biogenic amines by LC-tandem mass spectrometry and F NMR.
[So] Source:Food Chem;239:225-233, 2018 Jan 15.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:3,5-Bis-(trifluoromethyl)phenyl isothiocyanate, was used as a convenient reagent for the derivatization of histamine, tyramine, tryptamine and 2-phenylethylamine, which eliminates the purification step. The obtained derivatives were determined by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Additionally, the total amount of these amines was determined by F nuclear magnetic resonance analysis. The procedures were optimized and validated for linearity, limit of detection and quantification, intra- and inter-day precision and recovery resulting in good reproducibility and accuracy. The reagent was applied for determination of the above mentioned biogenic amines in beverages, and permitted an undemanding separation and determination of the derivatives. Moreover, it is a convenient reagent for analysis of the total amine content by quantitative F NMR.
[Mh] Termos MeSH primário: Aminas Biogênicas/análise
[Mh] Termos MeSH secundário: Cromatografia Líquida de Alta Pressão
Isotiocianatos
Reprodutibilidade dos Testes
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biogenic Amines); 0 (Isothiocyanates); 0D58F84LSU (phenylisothiocyanate)
[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:170907
[St] Status:MEDLINE


  8 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29061805
[Au] Autor:Ma YS; Hsiao YT; Lin JJ; Liao CL; Lin CC; Chung JG
[Ad] Endereço:School of Chinese Medicine for Post-Baccalaureate, I-Shou University, Kaohsiung, Taiwan, R.O.C.
[Ti] Título:Phenethyl Isothiocyanate (PEITC) and Benzyl Isothiocyanate (BITC) Inhibit Human Melanoma A375.S2 Cell Migration and Invasion by Affecting MAPK Signaling Pathway .
[So] Source:Anticancer Res;37(11):6223-6234, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Numerous evidence has shown that PEITC and BITC inhibit cancer cell migration and invasion. In this study, we investigated the anti-metastatic mechanisms of PEITC and BITC in human melanoma cancer A375.S2 cells in vitro. MATERIALS AND METHODS: We used a cell viability assay, an in-vitro scratch wound healing assay, a transwell assay for cell migration and invasion, a gelatin zymography assay, western blotting and EMSA to examine the anti-metastatic mechanisms of PEITC and BITC in A375.S2 cells. RESULTS: Sublethal concentrations of PEITC (0, 1, 2 and 2.5 µM) and BITC (0, 0.5, 1 and 2 µM) inhibited mobility, migration and invasion of A375.S2 cells that were assayed by wound healing and Transwell filter. PEITC and BITC inhibited MMP-2 activity in A375.S2 cells, as assessed by gelatin zymography assay. Results from western blotting indicated that PEITC (2.5 µM) and BITC (2 µM) decreased the levels of p-p38 following 24 and 48 h treatment. PEITC (1-2.5 µM) reduced the levels of p-JNK1/2 proteins following 48-h treatment but BITC increased p-JNK1/2 levels following 24-h treatment. PEITC (2.5 µM) reduced the levels of p-ERK1/2 proteins following 48-h treatment but BITC (0.5-2 µM) increased p-ERK1/2 levels following 24- and 48-h treatment. PEITC and BITC affect cell migration and invasion of A375.S2 cells via MAPK pathway. PEITC and BITC inhibited MMP-2 activity. PEITC increased NF-κB expression but BITC decreased NF-κB expression in the nucleus. Furthermore, NF-κB p65 binding to DNA was decreased following 2.5 µM PEITC treatment, but increased following treatment with 1-2 µM. However, 0.5-2 µM BITC treatment decreased the binding of NF-κB to DNA in A375.S2 cells, as assessed by electrophoretic mobility shift (EMSA) assay. CONCLUSION: Based on these observations, we suggest that PEITC and BITC can be used as anti-metastastic agents of human melanoma cells in the future.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Movimento Celular/efeitos dos fármacos
Isotiocianatos/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Melanoma/patologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Técnicas In Vitro
Melanoma/tratamento farmacológico
Melanoma/metabolismo
NF-kappa B/metabolismo
Invasividade Neoplásica
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Isothiocyanates); 0 (NF-kappa B); 6U7TFK75KV (phenethyl isothiocyanate); 871J6YOR8Q (benzyl isothiocyanate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  9 / 3523 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28947488
[Au] Autor:Redondo A; Chamorro PAF; Riego G; Leánez S; Pol O
[Ad] Endereço:Grup de Neurofarmacologia Molecular, Institut d'Investigació Biomèdica Sant Pau & Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona, Spain.
[Ti] Título:Treatment with Sulforaphane Produces Antinociception and Improves Morphine Effects during Inflammatory Pain in Mice.
[So] Source:J Pharmacol Exp Ther;363(3):293-302, 2017 Dec.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The activation of nuclear factor erythroid 2-related factor 2 (Nrf2) exerts potent antioxidative and anti-inflammatory effects; however, its participation in the modulation of chronic inflammatory pain and on the antinociceptive effects of -opioid receptor (MOR) agonists has not been evaluated. We investigated whether the induction of Nrf2 could alleviate chronic inflammatory pain and augment the analgesic effects of morphine and mechanisms implicated. In male C57BL/6 mice with inflammatory pain induced by complete Freund's adjuvant (CFA) subplantarly administered, we assessed: 1) antinociceptive actions of the administration of 5 and 10 mg/kg of a Nrf2 activator, sulforaphane (SFN); and 2) effects of SFN on the antinociceptive actions of morphine and on protein levels of Nrf2, heme oxygenase 1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1) enzymes, microglial activation and inducible nitric oxide synthase (NOS2) overexpression, as well as on mitogen-activated protein kinase (MAPK) and MOR expression in the spinal cord and paw of animals with inflammatory pain. Results showed that treatment with SFN inhibited allodynia and hyperalgesia induced by CFA and increased the local antinociceptive actions of morphine. This treatment also augmented the expression of Nrf2, HO-1, NQO1, and MOR, and inhibited NOS2 and CD11b/c overexpression and MAPK phosphorylation induced by inflammation. Thus, this study shows that the induction of Nrf2 might inhibit inflammatory pain and enhance the analgesic effects of morphine by inhibiting oxidative stress and inflammatory responses induced by peripheral inflammation. This study suggests the administration of SFN alone and in combination with morphine are potential new ways of treating chronic inflammatory pain.
[Mh] Termos MeSH primário: Analgésicos Opioides/administração & dosagem
Analgésicos/administração & dosagem
Dor Crônica/tratamento farmacológico
Isotiocianatos/administração & dosagem
Morfina/administração & dosagem
Fator 2 Relacionado a NF-E2/biossíntese
[Mh] Termos MeSH secundário: Animais
Dor Crônica/induzido quimicamente
Dor Crônica/metabolismo
Quimioterapia Combinada
Adjuvante de Freund/toxicidade
Inflamação/induzido quimicamente
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fator 2 Relacionado a NF-E2/agonistas
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Analgesics, Opioid); 0 (Isothiocyanates); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 76I7G6D29C (Morphine); 9007-81-2 (Freund's Adjuvant); GA49J4310U (sulforafan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.244376


  10 / 3523 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28922365
[Au] Autor:Kim Y; Wu AG; Jaja-Chimedza A; Graf BL; Waterman C; Verzi MP; Raskin I
[Ad] Endereço:Nutrasorb, LLC., Freehold, New Jersey, United States of America.
[Ti] Título:Isothiocyanate-enriched moringa seed extract alleviates ulcerative colitis symptoms in mice.
[So] Source:PLoS One;12(9):e0184709, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Moringa (Moringa oleifera Lam.) seed extract (MSE) has anti-inflammatory and antioxidant activities. We investigated the effects of MSE enriched in moringa isothiocyanate-1 (MIC-1), its putative bioactive, on ulcerative colitis (UC) and its anti-inflammatory/antioxidant mechanism likely mediated through Nrf2-signaling pathway. Dextran sulfate sodium (DSS)-induced acute (n = 8/group; 3% DSS for 5 d) and chronic (n = 6/group; cyclic rotations of 2.5% DSS/water for 30 d) UC was induced in mice that were assigned to 4 experimental groups: healthy control (water/vehicle), disease control (DSS/vehicle), MSE treatment (DSS/MSE), or 5-aminosalicyic acid (5-ASA) treatment (positive control; DSS/5-ASA). Following UC induction, water (vehicle), 150 mg/kg MSE, or 50 mg/kg 5-ASA were orally administered for 1 or 2 wks. Disease activity index (DAI), spleen/colon sizes, and colonic histopathology were measured. From colon and/or fecal samples, pro-inflammatory biomarkers, tight-junction proteins, and Nrf2-mediated enzymes were analyzed at protein and/or gene expression levels. Compared to disease control, MSE decreased DAI scores, and showed an increase in colon lengths and decrease in colon weight/length ratios in both UC models. MSE also reduced colonic inflammation/damage and histopathological scores (modestly) in acute UC. MSE decreased colonic secretions of pro-inflammatory keratinocyte-derived cytokine (KC), tumor necrosis factor (TNF)-α, nitric oxide (NO), and myeloperoxidase (MPO) in acute and chronic UC; reduced fecal lipocalin-2 in acute UC; downregulated gene expression of pro-inflammatory interleukin (IL)-1, IL-6, TNF-α, and inducible nitric oxide synthase (iNOS) in acute UC; upregulated expression of claudin-1 and ZO-1 in acute and chronic UC; and upregulated GSTP1, an Nrf2-mediated phase II detoxifying enzyme, in chronic UC. MSE was effective in mitigating UC symptoms and reducing UC-induced colonic pathologies, likely by suppressing pro-inflammatory biomarkers and increasing tight-junction proteins. This effect is consistent with Nrf2-mediated anti-inflammatory/antioxidant signaling pathway documented for other isothiocyanates similar to MIC-1. Therefore, MSE, enriched with MIC-1, may be useful in prevention and treatment of UC.
[Mh] Termos MeSH primário: Colite Ulcerativa/tratamento farmacológico
Colite Ulcerativa/metabolismo
Isotiocianatos/farmacologia
Moringa/química
Extratos Vegetais/farmacologia
Sementes/química
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Claudina-1/metabolismo
Colite Ulcerativa/induzido quimicamente
Colite Ulcerativa/patologia
Colo/metabolismo
Colo/patologia
Citocinas/metabolismo
Sulfato de Dextrana/toxicidade
Isotiocianatos/química
Lipocalina-2/metabolismo
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/metabolismo
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Peroxidase/metabolismo
Extratos Vegetais/química
Baço/metabolismo
Baço/patologia
Junções Íntimas/metabolismo
Junções Íntimas/patologia
Proteína da Zônula de Oclusão-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-1); 0 (Cldn1 protein, mouse); 0 (Cytokines); 0 (Isothiocyanates); 0 (Lipocalin-2); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Plant Extracts); 0 (Tjp1 protein, mouse); 0 (Zonula Occludens-1 Protein); 126469-30-5 (Lcn2 protein, mouse); 3129-90-6 (isothiocyanic acid); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 1.11.1.7 (Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184709



página 1 de 353 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde