Base de dados : MEDLINE
Pesquisa : D02.355.291.411 [Categoria DeCS]
Referências encontradas : 8310 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 831 ir para página                         

  1 / 8310 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441915
[Au] Autor:Cao L-; Yan M; Ma YX; Zhang BK; Fang PF; Xiang DX; Li ZH; Gong H; Deng Y; Li HD
[Ti] Título:Isoliquiritigenin protects against triptolide-induced hepatotoxicity in mice through Nrf2 activation.
[So] Source:Pharmazie;71(7):394-397, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Isoliquiritigenin, a flavonoid found in licorice, has been considered as an antioxidive and hepato-protective agent. Recent studies have shown that a possible mechanism for triptolide-induced hepatotoxicity is related to oxidative damage induced by reactive oxygen species. This study was done to investigate the protection effect of isoliquiritigenin against triptolide-induced hepatotoxicity and the mechanism involved. An acute liver injury model was established by intraperitoneal injection of triptolide (1.0 mg · kg-1) in mice. Different doses of isoliquiritigenin (12.5, 25 and 50 mg · kg-1) were employed as protection. The activities of AST, ALT, ALP and LDH in serum and levels of GSH, GPx, SOD, CAT and MDA in liver tissue were detected. The histopathological changes of liver tissues were observed after HE staining. The protein expression of Nrf2 was detected by western blot. Pretreatment with isoliquiritigenin significantly prevented the triptolide-induced hepatotoxicity indicated by reduced activities of AST, ALT, ALP and LDH. Moreover, isoliquiritigenin pretreatment also prevented from triptolide-induced hepatotoxicity by inhibiting MDA and restoring the levels of GSH, GPx, SOD and CAT. In addition, isoliquiritigenin could attenuate histopathological changes induced by triptolide. Furthermore, the results indicated that isoliquiritigenin pretreatment caused an increase in the protein expression of Nrf2. These results indicated that isoliquiritigenin could protect against triptolide-induced hepatotoxicity via activation of the Nrf2 pathway.
[Mh] Termos MeSH primário: Chalconas/farmacologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Diterpenos/antagonistas & inibidores
Diterpenos/toxicidade
Fator 2 Relacionado a NF-E2/metabolismo
Fenantrenos/antagonistas & inibidores
Fenantrenos/toxicidade
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/patologia
Compostos de Epóxi/antagonistas & inibidores
Compostos de Epóxi/toxicidade
Fígado/efeitos dos fármacos
Fígado/metabolismo
Testes de Função Hepática
Masculino
Malondialdeído/antagonistas & inibidores
Camundongos
Camundongos Endogâmicos ICR
Fator 2 Relacionado a NF-E2/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chalcones); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Phenanthrenes); 0 (Protective Agents); 19ALD1S53J (triptolide); 4Y8F71G49Q (Malondialdehyde); B9CTI9GB8F (isoliquiritigenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6535


  2 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460475
[Au] Autor:Song JM; Molla K; Anandharaj A; Cornax I; O Sullivan MG; Kirtane AR; Panyam J; Kassie F
[Ad] Endereço:Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
[Ti] Título:Triptolide suppresses the in vitro and in vivo growth of lung cancer cells by targeting hyaluronan-CD44/RHAMM signaling.
[So] Source:Oncotarget;8(16):26927-26940, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Higher levels of hyaluronan (HA) and its receptors CD44 and RHAMM have been associated with poor prognosis and metastasis in NSCLC. In the current study, our goal was to define, using cellular and orthotopic lung tumor models, the role of HA-CD44/RHAMM signaling in lung carcinogenesis and to assess the potential of triptolide to block HA-CD44/RHAMM signaling and thereby suppress the development and progression of lung cancer. Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP. Silencing of HAS2, CD44 or RHAMM induced similar effects. Addition of excess HA to the culture media completely abrogated the effects of triptolide and siRNAs targeting HAS2, CD44, or RHAMM. In an orthotopic lung cancer model in nude rats, intranasal administration of liposomal triptolide (400 µg/kg) for 8 weeks significantly reduced lung tumor growth as determined by bioluminescence imaging, lung weight measurements and gross and histopathological analysis of tumor burden. Also, triptolide suppressed expressions of Ki-67, a marker for cell proliferation, HAS2, HAS3, HA, CD44, and RHAMM in lung tumors. Overall, our results provide a strong rationale for mitigating lung cancer by targeting the HA-CD44/RHAMM signaling axis.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Diterpenos/farmacologia
Proteínas da Matriz Extracelular/metabolismo
Receptores de Hialuronatos/antagonistas & inibidores
Receptores de Hialuronatos/metabolismo
Neoplasias Pulmonares/metabolismo
Fenantrenos/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Compostos de Epóxi/farmacologia
Inativação Gênica
Seres Humanos
Receptores de Hialuronatos/genética
Hialuronan Sintases/genética
Hialuronan Sintases/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
RNA Interferente Pequeno/genética
Ratos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CD44 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (Phenanthrenes); 0 (RNA, Small Interfering); 0 (hyaluronan-mediated motility receptor); 19ALD1S53J (triptolide); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15879


  3 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29195901
[Au] Autor:Chen H; Chen Q; Jiang CM; Shi GY; Sui BW; Zhang W; Yang LZ; Li ZY; Liu L; Su YM; Zhao WC; Sun HQ; Li ZZ; Fu Z
[Ad] Endereço:Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China; China International Science and Technology Cooperation base of Child development and Critical Disorders, China; Chongqing Engineeri
[Ti] Título:Triptolide suppresses paraquat induced idiopathic pulmonary fibrosis by inhibiting TGFB1-dependent epithelial mesenchymal transition.
[So] Source:Toxicol Lett;284:1-9, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Idiopathic pulmonary fibrosis (IPF) and tumor are highly similar to abnormal cell proliferation that damages the body. This malignant cell evolution in a stressful environment closely resembles that of epithelial-mesenchymal transition (EMT). As a popular EMT-inducing factor, TGFß plays an important role in the progression of multiple diseases. However, the drugs that target TGFB1 are limited. In this study, we found that triptolide (TPL), a Chinese medicine extract, exerts an anti-lung fibrosis effect by inhibiting the EMT of lung epithelial cells. In addition, triptolide directly binds to TGFß and subsequently increase E-cadherin expression and decrease vimentin expression. In in vivo studies, TPL improves the survival state and inhibits lung fibrosis in mice. In summary, this study revealed the potential therapeutic effect of paraquat induced TPL in lung fibrosis by regulating TGFß-dependent EMT progression.
[Mh] Termos MeSH primário: Diterpenos/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Fibrose Pulmonar Idiopática/prevenção & controle
Paraquat/toxicidade
Fenantrenos/uso terapêutico
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Modelos Animais de Doenças
Diterpenos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Compostos de Epóxi/farmacologia
Compostos de Epóxi/uso terapêutico
Seres Humanos
Fibrose Pulmonar Idiopática/induzido quimicamente
Fibrose Pulmonar Idiopática/metabolismo
Fibrose Pulmonar Idiopática/patologia
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Camundongos
Simulação de Acoplamento Molecular
Fenantrenos/farmacologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diterpenes); 0 (Drugs, Chinese Herbal); 0 (Epoxy Compounds); 0 (Phenanthrenes); 0 (Tgfb1 protein, mouse); 0 (Transforming Growth Factor beta1); 19ALD1S53J (triptolide); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


  4 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29338026
[Au] Autor:Vanzyl EJ; Rick KRC; Blackmore AB; MacFarlane EM; McKay BC
[Ad] Endereço:Department of Biology, Carleton University, Ottawa ON, Canada.
[Ti] Título:Flow cytometric analysis identifies changes in S and M phases as novel cell cycle alterations induced by the splicing inhibitor isoginkgetin.
[So] Source:PLoS One;13(1):e0191178, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The spliceosome is a large ribonucleoprotein complex that catalyzes the removal of introns from RNA polymerase II-transcribed RNAs. Spliceosome assembly occurs in a stepwise manner through specific intermediates referred to as pre-spliceosome complexes E, A, B, B* and C. It has been reported that small molecule inhibitors of the spliceosome that target the SF3B1 protein component of complex A lead to the accumulation of cells in the G1 and G2/M phases of the cell cycle. Here we performed a comprehensive flow cytometry analysis of the effects of isoginkgetin (IGG), a natural compound that interferes with spliceosome assembly at a later step, complex B formation. We found that IGG slowed cell cycle progression in multiple phases of the cell cycle (G1, S and G2) but not M phase. This pattern was somewhat similar to but distinguishable from changes associated with an SF3B1 inhibitor, pladienolide B (PB). Both drugs led to a significant decrease in nascent DNA synthesis in S phase, indicative of an S phase arrest. However, IGG led to a much more prominent S phase arrest than PB while PB exhibited a more pronounced G1 arrest that decreased the proportion of cells in S phase as well. We also found that both drugs led to a comparable decrease in the proportion of cells in M phase. This work indicates that spliceosome inhibitors affect multiple phases of the cell cycle and that some of these effects vary in an agent-specific manner despite the fact that they target splicing at similar stages of spliceosome assembly.
[Mh] Termos MeSH primário: Biflavonoides/farmacologia
Divisão Celular/efeitos dos fármacos
Processamento de RNA/efeitos dos fármacos
Fase S/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Replicação do DNA/efeitos dos fármacos
Compostos de Epóxi/farmacologia
Citometria de Fluxo
Células HCT116
Seres Humanos
Macrolídeos/farmacologia
Precursores de RNA/metabolismo
Spliceossomos/efeitos dos fármacos
Spliceossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biflavonoids); 0 (Epoxy Compounds); 0 (Macrolides); 0 (RNA Precursors); 0 (isoginkgetin); 0 (pladienolide B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191178


  5 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29330051
[Au] Autor:Li X; Lu Q; Xie W; Wang Y; Wang G
[Ad] Endereço:Department of Orthopedics, Wuhan 672 Integrated Traditional Chinese and Western Medicine Hospital, Wuhan, 430079, Hubei, China. Electronic address: lixuguiwuhan@sina.com.
[Ti] Título:Anti-tumor effects of triptolide on angiogenesis and cell apoptosis in osteosarcoma cells by inducing autophagy via repressing Wnt/ß-Catenin signaling.
[So] Source:Biochem Biophys Res Commun;496(2):443-449, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteosarcoma is a common malignant bone tumor occurring in adolescents and children. The poor prognosis and low 5-year survival rate of osteosarcoma partly due to high metastasis of osteosarcoma. Triptolide (TPL), an extract from Tripterygium wilfordii, is widely used in cancer treatment. In our present study, we aimed to study the effect of TPL in osteosarcoma treatment and explore the associated regulation mechanism. Our study revealed that TPL inhibited angiogenesis by suppressing the expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in dose dependent manner. Besides, cell apoptosis was induced by TPL obviously in dose dependent manner. Further study demonstrated that TPL induced obvious cell autophagy with increased concentration. The cooperation of autophagy inhibitor 3-MA abolished the effect of TPL on anti-angiogenesis and apoptosis promoting. Moreover, we found that Wnt/ß-Catenin signaling was inactivated by TPL and the adding of pathway inducer Licl neutralized the effect of TPL on autophagy induction, anti-angiogenesis and apoptosis promoting. Taken together, we suggested that TPL inhibited angiogenesis and induced cell apoptosis in osteosarcoma cells by inducing autophagy via repressing Wnt/ß-Catenin signaling.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Autofagia/efeitos dos fármacos
Diterpenos/farmacologia
Regulação Neoplásica da Expressão Gênica
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Fenantrenos/farmacologia
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/farmacologia
Apoptose/efeitos dos fármacos
Autofagia/genética
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Compostos de Epóxi/farmacologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Cloreto de Lítio/farmacologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteoblastos/patologia
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CTNNB1 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Phenanthrenes); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); 19ALD1S53J (triptolide); 5142-23-4 (3-methyladenine); G4962QA067 (Lithium Chloride); JAC85A2161 (Adenine)
[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:180114
[St] Status:MEDLINE


  6 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29288766
[Au] Autor:Wang J; Zhang Z; Li R; Sun W; Chen J; Zhang H; Shu K; Lei T
[Ad] Endereço:Sino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
[Ti] Título:Triptolide inhibits pituitary adenoma cell viability, migration and invasion via ADAM12/EGFR signaling pathway.
[So] Source:Life Sci;194:150-156, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: Triptolide, an effective component derived from Tripterygium wilfordii, has been well recognized to process a broad-spectrum antitumor activities in various tumor types. However, the potential role of triptolide in pituitary adenomas remains unknown. The aim of this study was to investigate the precise role of triptolide and underlying mechanism in regulating pituitary adenoma cell viability, migration and invasion. MAIN METHODS: We use mouse pituitary adenoma cells (TtT/GF and AtT20 cells) as the experiment model and treated them with varying concentrations of triptolide. The corresponding inhibitory effects on cell viability, migration, invasion and apoptosis were examined respectively, and the underlying mechanism was determined by investigating ADAM12 (a disintegrin and metalloprotease 12)/EGFR signaling. KEY FINDINGS: Triptolide significantly inhibited cell viability, migration and invasion in TtT/GF and AtT20 cells in a dose-dependent manner. Mechanistically, triptolide significantly reduced ADAM12 expression at protein levels and attenuated ADAM12/EGFR signaling. Meanwhile, triptolide treatment combined with ADAM12 silencing enhanced the suppression effects on cell viability, migration and invasion, and those effects were restored following ADAM12-rescued. Moreover, triptolide suppressed the tumorigenesis of TtT/GF and AtT20 cells in vivo. SIGNIFICANCE: Our research provides evidence that triptolide inhibits pituitary adenoma cell viability, migration and invasion via ADAM12/EGFR signaling pathway. These findings suggest a potential role for triptolide in treating pituitary adenomas.
[Mh] Termos MeSH primário: Proteína ADAM12/metabolismo
Adenoma/dietoterapia
Antineoplásicos Alquilantes/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Diterpenos/farmacologia
Fenantrenos/farmacologia
Neoplasias Hipofisárias/tratamento farmacológico
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Adenoma/patologia
Animais
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Compostos de Epóxi/farmacologia
Camundongos
Hipófise/efeitos dos fármacos
Hipófise/metabolismo
Hipófise/patologia
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Phenanthrenes); 19ALD1S53J (triptolide); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.24.- (ADAM12 Protein)
[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:171231
[St] Status:MEDLINE


  7 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29293497
[Au] Autor:Marín de Mas I; Aguilar E; Zodda E; Balcells C; Marin S; Dallmann G; Thomson TM; Papp B; Cascante M
[Ad] Endereço:Department of Biochemistry and Molecular Biomedicine, Faculty of Biology, Universitat de Barcelona, Barcelona, Spain.
[Ti] Título:Model-driven discovery of long-chain fatty acid metabolic reprogramming in heterogeneous prostate cancer cells.
[So] Source:PLoS Comput Biol;14(1):e1005914, 2018 01.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial-mesenchymal-transition promotes intra-tumoral heterogeneity, by enhancing tumor cell invasiveness and promoting drug resistance. We integrated transcriptomic data for two clonal subpopulations from a prostate cancer cell line (PC-3) into a genome-scale metabolic network model to explore their metabolic differences and potential vulnerabilities. In this dual cell model, PC-3/S cells express Epithelial-mesenchymal-transition markers and display high invasiveness and low metastatic potential, while PC-3/M cells present the opposite phenotype and higher proliferative rate. Model-driven analysis and experimental validations unveiled a marked metabolic reprogramming in long-chain fatty acids metabolism. While PC-3/M cells showed an enhanced entry of long-chain fatty acids into the mitochondria, PC-3/S cells used long-chain fatty acids as precursors of eicosanoid metabolism. We suggest that this metabolic reprogramming endows PC-3/M cells with augmented energy metabolism for fast proliferation and PC-3/S cells with increased eicosanoid production impacting angiogenesis, cell adhesion and invasion. PC-3/S metabolism also promotes the accumulation of docosahexaenoic acid, a long-chain fatty acid with antiproliferative effects. The potential therapeutic significance of our model was supported by a differential sensitivity of PC-3/M cells to etomoxir, an inhibitor of long-chain fatty acid transport to the mitochondria.
[Mh] Termos MeSH primário: Ácidos Graxos/metabolismo
Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Ácido Araquidônico/metabolismo
Transporte Biológico Ativo/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular
Biologia Computacional
Ácidos Docosa-Hexaenoicos/metabolismo
Eicosanoides/metabolismo
Transição Epitelial-Mesenquimal
Compostos de Epóxi/farmacologia
Ácidos Graxos/química
Seres Humanos
Masculino
Redes e Vias Metabólicas
Mitocôndrias/metabolismo
Modelos Biológicos
Invasividade Neoplásica
Neoplasias da Próstata/tratamento farmacológico
Neoplasias da Próstata/patologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Eicosanoids); 0 (Epoxy Compounds); 0 (Fatty Acids); 25167-62-8 (Docosahexaenoic Acids); 27YG812J1I (Arachidonic Acid); MSB3DD2XP6 (etomoxir)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005914


  8 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460114
[Au] Autor:Reynolds HT; Slot JC; Divon HH; Lysøe E; Proctor RH; Brown DW
[Ad] Endereço:Department of Plant Pathology, The Ohio State University, Columbus, OH.
[Ti] Título:Differential Retention of Gene Functions in a Secondary Metabolite Cluster.
[So] Source:Mol Biol Evol;34(8):2002-2015, 2017 Aug 01.
[Is] ISSN:1537-1719
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In fungi, distribution of secondary metabolite (SM) gene clusters is often associated with host- or environment-specific benefits provided by SMs. In the plant pathogen Alternaria brassicicola (Dothideomycetes), the DEP cluster confers an ability to synthesize the SM depudecin, a histone deacetylase inhibitor that contributes weakly to virulence. The DEP cluster includes genes encoding enzymes, a transporter, and a transcription regulator. We investigated the distribution and evolution of the DEP cluster in 585 fungal genomes and found a wide but sporadic distribution among Dothideomycetes, Sordariomycetes, and Eurotiomycetes. We confirmed DEP gene expression and depudecin production in one fungus, Fusarium langsethiae. Phylogenetic analyses suggested 6-10 horizontal gene transfers (HGTs) of the cluster, including a transfer that led to the presence of closely related cluster homologs in Alternaria and Fusarium. The analyses also indicated that HGTs were frequently followed by loss/pseudogenization of one or more DEP genes. Independent cluster inactivation was inferred in at least four fungal classes. Analyses of transitions among functional, pseudogenized, and absent states of DEP genes among Fusarium species suggest enzyme-encoding genes are lost at higher rates than the transporter (DEP3) and regulatory (DEP6) genes. The phenotype of an experimentally-induced DEP3 mutant of Fusarium did not support the hypothesis that selective retention of DEP3 and DEP6 protects fungi from exogenous depudecin. Together, the results suggest that HGT and gene loss have contributed significantly to DEP cluster distribution, and that some DEP genes provide a greater fitness benefit possibly due to a differential tendency to form network connections.
[Mh] Termos MeSH primário: Alcadienos/metabolismo
Compostos de Epóxi/metabolismo
Álcoois Graxos/metabolismo
Genoma Fúngico/genética
Família Multigênica/genética
[Mh] Termos MeSH secundário: Ascomicetos/genética
Bases de Dados de Ácidos Nucleicos
Evolução Molecular
Proteínas Fúngicas/genética
Fusarium/genética
Perfilação da Expressão Gênica/métodos
Regulação Fúngica da Expressão Gênica/genética
Transferência Genética Horizontal/genética
Filogenia
Metabolismo Secundário/genética
Virulência/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkadienes); 0 (Epoxy Compounds); 0 (Fatty Alcohols); 0 (Fungal Proteins); 139508-73-9 (depudecin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1093/molbev/msx145


  9 / 8310 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29273563
[Au] Autor:Olas B; Brys M
[Ad] Endereço:Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland. Electronic address: beata.olas@biol.uni.lodz.pl.
[Ti] Título:Is it safe to use Acorus calamus as a source of promising bioactive compounds in prevention and treatment of cardiovascular diseases?
[So] Source:Chem Biol Interact;281:32-36, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Acorus calamus has a rich history in natural medicine, and offers many health benefits. The plant has anti-inflammatory, antimicrobial, diuretic, antiurolithiatic and other properties. Moreover, various parts, especially the rhizome and roots, are sources of a range of bioactive phenolic compounds with beneficial effects on the cardiovascular system. This review article summarizes the current knowledge of the chemical composition of different parts of A. calamus and their roles in the prevention and treatment of cardiovascular diseases. However, as no human studies have been performed, the review only includes in vitro and animal studies. The paper also briefly reviews the toxicity of A. calamus and its products for human health, especially regarding the cardiovascular system.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Óleos Voláteis/uso terapêutico
[Mh] Termos MeSH secundário: Acorus/química
Acorus/metabolismo
Animais
Anisóis/química
Anisóis/metabolismo
Anisóis/uso terapêutico
Peso Corporal/efeitos dos fármacos
Doenças Cardiovasculares/tratamento farmacológico
Compostos de Epóxi/química
Compostos de Epóxi/metabolismo
Compostos de Epóxi/toxicidade
Seres Humanos
Hipolipemiantes/química
Hipolipemiantes/uso terapêutico
Óleos Voláteis/química
Óleos Voláteis/metabolismo
Fenóis/química
Fenóis/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anisoles); 0 (Epoxy Compounds); 0 (Hypolipidemic Agents); 0 (Oils, Volatile); 0 (Phenols); 0 (asarone)
[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:171224
[St] Status:MEDLINE


  10 / 8310 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29227079
[Au] Autor:Kоbyli nska LI; Havrylyuk DY; Mitina NE; Zaichenko AS; Lesyk RB; Zіme nkovsky BS; Stoika RS
[Ti] Título:Biochemical indicators of nephrotoxicity in blood serum of rats treated with novel 4-thiazolidinone derivatives or their complexes with polyethylene glycol-containing nanoscale polymeric carrier
[So] Source:Ukr Biochem J;88(1):51-60, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to compare the effect of new synthetic 4-thiazolidinone derivatives (potential anticancer compounds denoted as 3882, 3288 and 3833) and doxorubicin (positive control) in free form and in their complexes with synthetic polyethylene glycol-containing nanoscale polymeric carrier on the biochemical indicators of nephrotoxicity in blood serum of rats. The concentration of total protein, urea, creatinine, glucose, ions of sodium, potassium, calcium, iron and chloride was measured. It was found that after injection of the investigated compounds, the concentration of sodium cations and chloride anions in blood serum was increased compared with control (untreated animals). Doxorubicin's injection was accompanied by a decrease in the concentration of iron cations. The concentration of total protein, urea and creatinine decreased under the influence of the studied compounds. Complexation of these аntineoplastic substances with a synthetic polymeric nanocarrier lowered the concentration of the investigated metabolites substantially compared to the effect of these compounds in free form. The normalization of concentration of total protein, urea and creatinine in blood serum of rats treated with complexes of the studied compounds with the polymeric carrier comparing with increased concentration of these indicators at the introduction of such compounds in free form was found.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Rim/efeitos dos fármacos
Nanoestruturas/administração & dosagem
Polietilenoglicóis/química
Tiazolidinas/toxicidade
[Mh] Termos MeSH secundário: Animais
Animais não Endogâmicos
Antineoplásicos/síntese química
Glicemia/metabolismo
Proteínas Sanguíneas/metabolismo
Cálcio/sangue
Cloretos/sangue
Creatinina/sangue
Doxorrubicina/toxicidade
Portadores de Fármacos/administração & dosagem
Compostos de Epóxi/química
Ferro/sangue
Rim/metabolismo
Masculino
Metacrilatos/química
Nanoestruturas/química
Poliacetilenos/química
Potássio/sangue
Ratos
Sódio/sangue
Tiazolidinas/síntese química
Testes de Toxicidade Aguda
Ureia/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Blood Glucose); 0 (Blood Proteins); 0 (Chlorides); 0 (Drug Carriers); 0 (Epoxy Compounds); 0 (Methacrylates); 0 (Thiazolidines); 25067-58-7 (Polyacetylenes); 30IQX730WE (Polyethylene Glycols); 80168379AG (Doxorubicin); 8W8T17847W (Urea); 9NEZ333N27 (Sodium); AYI8EX34EU (Creatinine); E1UOL152H7 (Iron); R8WN29J8VF (glycidyl methacrylate); RWP5GA015D (Potassium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.051



página 1 de 831 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