Base de dados : MEDLINE
Pesquisa : D08.811.277.656.300.480.205.352 [Categoria DeCS]
Referências encontradas : 12696 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1270 ir para página                         

  1 / 12696 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441919
[Au] Autor:Lim HW; Kim K; Lim CJ
[Ti] Título:Contribution of ginsenoside Re to cellular redox homeostasis via upregulating glutathione and superoxide dismutase in HaCaT keratinocytes under normal conditions.
[So] Source:Pharmazie;71(7):413-419, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Re (Re) is one of the main ginsenosides which are known to be responsible for diverse pharmacological properties of ginseng, widely used as a dietary supplement and a general tonic. The present work was undertaken to evaluate the antioxidative property of Re by analyzing reactive oxygen species (ROS), nitric oxide (NO), pro-matrix metalloproteinase-2 (proMMP-2) and -9 (proMMP-9), total glutathione (GSH) and superoxide dismutase (SOD) in normal, unstressed HaCaT keratinocytes. When HaCaT cells were subjected to Re, Re suppressed the ROS and NO levels in a concentration-dependent manner. Re at concentrations used exhibited no cytotoxicity on the cellular viabilities of HaCaT cells. It was also able to attenuate proMMP-2 and -9 at both activity and protein levels. On the contrary, Re was capable of enhancing the total GSH and SOD activity levels. The findings suggest that Re has an antioxidative property through the upregulation of some antioxidant components, including total GSH and SOD, in HaCaT keratinocytes, which then can play its underlying role in maintaining the cellular redox homeostasis.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Ginsenosídeos/farmacologia
Glutationa/biossíntese
Homeostase/efeitos dos fármacos
Queratinócitos/efeitos dos fármacos
Superóxido Dismutase/biossíntese
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Glutationa/efeitos dos fármacos
Seres Humanos
Metaloproteinase 2 da Matriz/efeitos dos fármacos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/efeitos dos fármacos
Metaloproteinase 9 da Matriz/metabolismo
Óxido Nítrico/antagonistas & inibidores
Oxirredução
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Ginsenosides); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); 46F3R0BL3I (ginsenoside Re); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); GAN16C9B8O (Glutathione)
[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.2016.6518


  2 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381400
[Au] Autor:Song ZY; Wang F; Cui SX; Qu XJ
[Ad] Endereço:a Department of Pharmacology, School of Basic Medical Sciences , Capital Medical University , Beijing , China.
[Ti] Título:Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/ß-Catenin Pathways.
[So] Source:Cancer Invest;36(1):10-18, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CXCL12 is an extracellular chemokine binding to cell surface receptor CXCR4. We found that activation of CXCL12/CXCR4 axis stimulated angiogenesis in endothelial cells. Knockdown of CXCR4 in endothelial cells prevented the branch points of angiogenesis. Endothelial cells exposed to CXCL12 presented high level of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase MMP-2, but not in CXCR4 knockdown cells. Further studies revealed that activation of CXCL12/CXCR4 axis in vascular endothelial cells stimulates the angiogenesis through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/ß-catenin pathways. Conclusion, downregulation of CXCR4 could inhibit angiogenesis in cancer tissues.
[Mh] Termos MeSH primário: Quimiocina CXCL12/genética
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica/genética
Neovascularização Patológica/genética
Receptores CXCR4/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Metaloproteinase 2 da Matriz/genética
Proteínas Quinases Ativadas por Mitógeno/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Receptor do Fator de Crescimento Epidérmico/genética
Regulação para Cima/genética
Fator A de Crescimento do Endotélio Vascular/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1422512


  3 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465354
[Au] Autor:Farabegoli F; Govoni M; Spisni E; Papi A
[Ad] Endereço:Department of Pharmacology and Biotechnology (FaBiT), University of Bologna, Bologna, Italy fulvia.farabegoli@unibo.it.
[Ti] Título:EGFR inhibition by (-)-epigallocatechin-3-gallate and IIF treatments reduces breast cancer cell invasion.
[So] Source:Biosci Rep;37(3), 2017 Jun 30.
[Is] ISSN:1573-4935
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Epidermal growth factor receptor (EGFR) expression is an important marker in breast carcinoma pathology and is considered a pivotal molecule for cancer cell proliferation, invasion and metastasis. We investigated the effects of epigallocatechin-3-gallate (EGCG), the most active green tea catechin, in combination with 6-OH-11-O-hydroxyphenanthrene (IIF), a synthetic retinoid X receptor-γ (RXRγ) agonist, on three breast carcinoma cell lines: MCF-7, MCF-7TAM and MDA-MB-231. EGFR and AKT activation and molecular markers of cell motility and migration (CD44, extracellular matrix metalloproteinase (MMP) inducer (EMMPRIN), MMP-2, MMP-9 and tissue inhibitor of metalloproteinases (TIMPs)) were studied after EGCG and IIF treatments. The EGCG + IIF treatment was the most active in down-regulating EGFR phosphorylation at Tyr in all the investigated cell lines; p473AKT was also down-regulated in MCF-TAM cells. EGCG + IIF was also the most active treatment in reducing the expression of markers of invasion and migration in all the three cell lines: CD44, EMMPRIN, MMP-2 and -9 expression decreased, whereas TIMPs were up-regulated. Zymography and scratch assay also confirmed the reduced invasion tendency. We considered that EGCG and IIF treatments could alter the molecular network based on EGFR, CD44 and EMMPRIN expression interdependence and reduced the migration tendency in MCF-7, MCF-7TAM and MDA-MB-231 cells. These events only occurred in association with AKT inactivation in MCF-7TAM cells. In conclusion, the combination of EGCG and IIF significantly attenuated the invasive behaviour of breast carcinoma cells.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Catequina/análogos & derivados
Movimento Celular/efeitos dos fármacos
Invasividade Neoplásica/patologia
Fenantrenos/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Basigina/metabolismo
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Catequina/farmacologia
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Feminino
Seres Humanos
Células MCF-7
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/efeitos dos fármacos
Inibidor Tecidual de Metaloproteinase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-OH-11-O-hydroxyphenanthrene); 0 (Phenanthrenes); 0 (Protein Kinase Inhibitors); 0 (Tissue Inhibitor of Metalloproteinase-1); 136894-56-9 (Basigin); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  4 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29346427
[Au] Autor:Teshima T; Matsumoto H; Koyama H
[Ad] Endereço:Laboratory of Veterinary Internal Medicine, Department of Veterinary Clinical Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Musashino-shi, Tokyo, Japan.
[Ti] Título:Soluble factors from adipose tissue-derived mesenchymal stem cells promote canine hepatocellular carcinoma cell proliferation and invasion.
[So] Source:PLoS One;13(1):e0191539, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The potential effects of adipose tissue-derived mesenchymal stem cells (AT-MSCs) on the growth and invasion of canine tumours including hepatocellular carcinoma (HCC) are not yet understood. Moreover in humans, the functional contribution of AT-MSCs to malignancies remains controversial. The purpose of this study was to investigate the effects of AT-MSCs on the proliferation and invasion of canine HCC cells in vitro. The effect of AT-MSCs on mRNA levels of factors related to HCC progression were also evaluated. Conditioned medium from AT-MSCs (AT-MSC-CM) significantly enhanced canine HCC cell proliferation and invasion. Moreover, mRNA expression levels of transforming growth factor-beta 1, epidermal growth factor A, hepatocyte growth factor, platelet-derived growth factor-beta, vascular endothelial growth factor, and insulin-like growth factor 2 were 2.3 ± 0.4, 2.0 ± 0.5, 5.7 ± 1.9, 1.7 ± 0.2, 2.1 ± 0.4, and 1.4 ± 0.3 times higher, respectively (P < 0.05). The mRNA expression level of MMP-2 also increased (to 4.0 ± 1.2 times control levels) in canine HCC cells co-cultured with AT-MSCs, but MMP-9 mRNA significantly decreased (to 0.5 ± 0.1 times control levels). These findings suggest that soluble factors from AT-MSCs promote the proliferation and invasion of canine HCC cells.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Carcinoma Hepatocelular/veterinária
Proliferação Celular
Doenças do Cão/metabolismo
Neoplasias Hepáticas/veterinária
Células Mesenquimais Estromais/metabolismo
Invasividade Neoplásica
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/enzimologia
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Meios de Cultivo Condicionados
Doenças do Cão/patologia
Cães
Feminino
Neoplasias Hepáticas/enzimologia
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Masculino
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 9 da Matriz/genética
Células Mesenquimais Estromais/citologia
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (RNA, Messenger); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[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:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191539


  5 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381911
[Au] Autor:Cheng J; Hao X; Zhang Z
[Ad] Endereço:Department of Ophthalmology, Aerospace Central Hospital, Beijing, China.
[Ti] Título:Risk of macular degeneration affected by polymorphisms in Matrix metalloproteinase-2: A case-control study in Chinese Han population.
[So] Source:Medicine (Baltimore);96(47):e8190, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to investigate the correlation of single nucleotide polymorphisms (SNPs) in Matrix metalloproteinase -2 (MMP-2) gene and the risk of age-related macular degeneration (AMD) in Chinese Han population.A total of 126 AMD patients and 141 healthy controls participated in this study. Genotypes of MMP-2 gene polymorphisms were identified by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). χtest was used to detect the differences of genotypes and alleles frequencies between case and control groups. Relative risk of AMD was evaluated by odds ratios (ORs) with 95% confidence intervals (CIs).Distribution of variant allele carriers (computed tomography + TT genotypes) of MMP-2 gene rs243865 SNP was significantly different between case and control groups, and might act as protective factors for the onset of AMD (P = .044, OR = 0.583, 95% CI = 0.344-0.987). Nevertheless, the T allele might reduce the AMD risk (P = .030, OR = 0.611, 95% CI = 0.390-0.956). However, no significant association existed between rs243865 and AMD risk in the subgroup analysis based on age. GA + AA genotypes of rs243866 SNP may associate with a decreased risk of AMD in the age≤65 years subgroup (P = .028, OR = 0.399, 95% CI = 0.174-0.915).MMP-2 gene rs243865 and rs243866 SNPs associated with the risk of AMD. Further studies should be performed to confirm the results.
[Mh] Termos MeSH primário: Degeneração Macular/epidemiologia
Metaloproteinase 2 da Matriz/genética
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
China/epidemiologia
Feminino
Frequência do Gene
Genótipo
Seres Humanos
Degeneração Macular/genética
Masculino
Meia-Idade
Razão de Chances
Reação em Cadeia da Polimerase
Polimorfismo de Fragmento de Restrição
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008190


  6 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29431064
[Au] Autor:Mathuram TL; Ravikumar V; Reece LM; Sasikumar CS; Cherian KM
[Ad] Endereço:Department of Stem Cell and Tissue Engineering, Frontier Mediville (A Unit of Frontier Lifeline and Dr. K. M. Cherian Heart Foundation), Affiliated to University of Madras, Chennai-601201, Tamil Nadu, India.
[Ti] Título:Correlative Studies Unravelling the Possible Mechanism of Cell Death in Tideglusib-Treated Human Ovarian Teratocarcinoma-Derived PA-1 Cells.
[So] Source:J Environ Pathol Toxicol Oncol;36(4):321-344, 2017.
[Is] ISSN:2162-6537
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aims to unravel the use of GSK-3 inhibitors as viable apoptotic inducers for teratocarcinoma-derived ovarian PA-1 cells. MTT assay was carried out to assess inhibitory concentrations of LiCl and TDG. AO/EB staining and Hoechst 33258 staining were employed to assess the damage. Mitochondrial membrane potential (ΔΨm) and ROS generation were assessed with IC50 concentrations of LiCl and TDG. Tumor-related genes (p53, p21, IL-8, TNF-α, MMP-2, Fas-L, Cox-2, and caspase-3) were assessed with 1/4 IC50, 1/2 IC50, IC50 concentrations by semi-quantitative RT- PCR. Cell cycle analysis was performed with IC50 concentration of LiCl and TDG. Western blot analysis was performed for caspase-3, caspase-7, caspase-9, PARP to estimate the possible damage induced by GSK-3 inhibitors and regulation of GSK-3ß, pGSK-3ß, Cox-2. GSK-3 inhibitors demonstrated a concentration and time-dependent reduction in cell viability, exhibiting significant ROS generation and reduced ΔΨm at their IC50 values. Substantial concentration-dependent gene expression changes with significant upregulation of P21, Cox-2, TNF-α, caspase-3, Fas-L were observed. Protein expression of caspase-3 caspase-7, caspase-9, PARP exhibited significant cleavage in LiCl and TDG-treated cells. Protein expression of Cox-2 was significantly increased in IC50 concentration of TDG. Cell cycle analysis showed significant accumulation of cells at sub-G0-G1.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Neoplasias Ovarianas/tratamento farmacológico
Teratocarcinoma/tratamento farmacológico
Tiadiazóis/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Inibidor de Quinase Dependente de Ciclina p21/genética
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Cloreto de Lítio/farmacologia
Metaloproteinase 2 da Matriz/genética
Potencial da Membrana Mitocondrial
Neoplasias Ovarianas/patologia
Espécies Reativas de Oxigênio/metabolismo
Teratocarcinoma/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (NP 031112); 0 (Reactive Oxygen Species); 0 (Thiadiazoles); EC 2.7.11.26 (Glycogen Synthase Kinase 3); EC 3.4.24.24 (Matrix Metalloproteinase 2); G4962QA067 (Lithium Chloride)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.1615/JEnvironPatholToxicolOncol.2017025018


  7 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29228922
[Au] Autor:Miao F; Zhang X; Cao Y; Wang Y; Zhang X
[Ad] Endereço:School of Basic Medical Sciences, Binzhou Medical University, 346 Guanhai Road, Yantai, Shandong, People's Republic of China.
[Ti] Título:Effect of siRNA-silencing of SALL2 gene on growth, migration and invasion of human ovarian carcinoma A2780 cells.
[So] Source:BMC Cancer;17(1):838, 2017 12 11.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The role of Spalt-like gene-2 (SALL2) in tumorigenesis remains incompletely elucidated. This study investigated the effects of SALL2 on human ovarian carcinoma (OC) A2780 cells and the probable mechanism. METHODS: Expression of SALL2 in human OC cell lines were detected by reverse transcription PCR (RT-PCR) and Western blot analysis. A2780 cells were transfected with small-interfering ribonucleic acid (siRNA) to silence SALL2. SALL2 expression was detected by RT-PCR, Western blot analysis and immunofluorescence assay. Cell proliferation was measured by CCK-8 assay and flow cytometry (FCM). Apoptosis was measured by FCM. Cell migration was detected by real-time cell analysis. Cell invasion was detected by transwell assay. mRNA expression of p21 was detected by quantitative real-time PCR. Western blot analysis was used to determine the expression of matrix metalloproteinase (MMP)2, MMP9, protein kinase B (PKB, also called Akt), and phosphorylated-Akt (p-Akt). RESULTS: SALL2 was expressed in six OC cell lines, and the expression was the highest in A2780 cells. Compared with that in the Scramble group, SALL2 expression in A2780 was downregulated after transfection with siRNA-2 and siRNA-3 for 48 h. Compared with that in the Scramble group, proliferation of A2780 cells in the siRNA-2 group increased after transfection for 24, 48 and 72 h. In the siRNA-2 group, the proportion of A2780 cells decreased in the G0/G1 phase, and cell apoptosis decreased after transfection for 48 h. Compared with that in the Scramble group, the cell migration and invasion abilities of A2780 cells increased. Compared with that in the Scramble group, p21 mRNA expression in A2780 cells decreased after transfection with siRNA2. When SALL2 was silenced, the expression of MMP2/9 and p-Akt in A2780 cells increased. Furthermore, the PI3K inhibitor LY294002 could effectively reversed SALL2 siRNA-induced phosphorylation of Akt, migration and invasion of A2780 cells. CONCLUSION: Transient silencing of SALL2 promotes cell proliferation, migration, and invasion, and inhibits apoptosis of A2780 cells. In SALL2 siRNA-silenced cells, p21 expression was decreased. SALL2 knockdown by siRNA induces the migration and invasion of A2780 cells; this phenomenon is possibly associated with the increased expression of MMP2/9 and the activation of the PI3K/Akt signalling pathway.
[Mh] Termos MeSH primário: Invasividade Neoplásica/genética
Neoplasias Ovarianas/genética
Interferência de RNA
RNA Interferente Pequeno/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Feminino
Seres Humanos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (RNA, Small Interfering); 0 (SALL2 protein, human); 0 (Transcription Factors); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3843-y


  8 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29225168
[Au] Autor:Chai H; Tao Z; Chen W; Xu Y; Huang F; Su C; Chen X
[Ad] Endereço:The Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Changle Road 68, Nanjing 210006, Jiangsu, People's Republic of China.
[Ti] Título:Cortistatin attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the ERK1/2 signaling pathways.
[So] Source:Biochem Biophys Res Commun;495(2):1801-1806, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) is a fatal disease that is associated with chronic inflammation in the vessel wall. Cortistatin is implicated in inflammation, vascular smooth muscle cell migration and other cardiovascular pathologies. But, the hypothetical effect of cortistatin on AAA remains uncertain. We investigated the effect of cortistatin administration to angiotensin (Ang) II-induced AAA formation in apolipoprotein E deficient (Apoe ) mice. We showed that cortistatin administration significantly suppresses incidence and severity of AAA in Apoe mice. A significant increase in macrophage infiltration, excretion of inflammatory cytokines, activities and expression levels of MMP2 and MMP9, reactive oxygen species levels and cell apoptosis in aneurysmal aortic wall of Apoe mice infused with Ang-II, and these events were significantly alleviated by co-treatment with cortistatin. Mechanistic studies showed that the protective effects of cortistatin were related to the blocking of ERK1/2 signaling pathways, while does not was not actually affect JNK, P38 phosphorylation. In conclusion, cortistatin appears to play an essential role in the formation of AAA and indicate cortistatin may as novel therapeutic option for AAA.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/prevenção & controle
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neuropeptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Animais
Aorta Abdominal/efeitos dos fármacos
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/etiologia
Aneurisma da Aorta Abdominal/metabolismo
Apoptose/efeitos dos fármacos
Linhagem Celular
Modelos Animais de Doenças
Elastina/metabolismo
Masculino
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Knockout para ApoE
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Proteólise/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Reactive Oxygen Species); 0 (cortistatin); 11128-99-7 (Angiotensin II); 9007-58-3 (Elastin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[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:171212
[St] Status:MEDLINE


  9 / 12696 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29288728
[Au] Autor:Ritter AMV; de Faria AP; Barbaro NR; Sabbatini AR; Corrêa NB; Brunelli V; Fattori A; Amorim R; Modolo R; Moreno H
[Ad] Endereço:Laboratory of Cardiovascular Pharmacology, School of Medical Sciences, University of Campinas, Campinas, SP, Brazil. Electronic address: ale_mileni@hotmail.com.
[Ti] Título:The rs243866/243865 polymorphisms in MMP-2 gene and the relationship with BP control in obese resistant hypertensive subjects.
[So] Source:Gene;646:129-135, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We sought to investigate whether the polymorphisms rs243865 (-1306C>T); rs243866 (-1575G>A) and rs2285053 (-735C>T) in metalloproteinases 2 - MMP-2 gene and rs17576 (Q279R), rs17577 (Q668R) and rs3918242 (-1562C>T) in MMP-9 gene are associated with clinical outcomes in obese resistant hypertensive (RH) subjects. One hundred and twenty RH were enrolled in this cross-sectional study and divided into obese (n=63) and non-obese (n=57) according to body mass index. Genotypes were determined by real-time PCR using TaqMan probes. We determined pulse wave velocity (PWV), microalbuminuria and left ventricular mass index (LVMI) to assess TODs. Obese and non-obese RH had similar allele, genotype and haplotype distributions for all polymorphisms assessed but obese RH subjects carrying the low frequency allele for SNPs in MMP-2 gene had higher ambulatory diastolic blood pressure. Also, PWV and LVMI were higher in subjects carrying the low frequency allele for SNPs in MMP-2 gene. Regarding MMP-9 gene, office diastolic BP levels were higher in the AA genotype individuals compared to the G allele group for rs17576 polymorphism, while the opposite was found regarding the microalbuminuria level. Independent multiple linear regression analyses revealed that both A allele for rs243865 and T allele for rs243866 in MMP-2 gene were associated with ambulatory diastolic levels in obese RH subjects, apart from potential confounders. Our study suggests that rs243866/rs243865 in the MMP-2 gene are related to BP levels in obese RH subjects, although TODs present in this population seem to be dependent of a combination of other factors besides the genetic polymorphisms.
[Mh] Termos MeSH primário: Hipertensão/genética
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 9 da Matriz/genética
Obesidade/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Idoso
Pressão Sanguínea
Estudos Transversais
Feminino
Predisposição Genética para Doença
Genótipo
Haplótipos
Seres Humanos
Masculino
Meia-Idade
Análise de Onda de Pulso
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  10 / 12696 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29225138
[Au] Autor:Jeong M; Kim HM; Ahn JH; Lee KT; Jang DS; Choi JH
[Ad] Endereço:Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, South Korea.
[Ti] Título:9-Hydroxycanthin-6-one isolated from stem bark of Ailanthus altissima induces ovarian cancer cell apoptosis and inhibits the activation of tumor-associated macrophages.
[So] Source:Chem Biol Interact;280:99-108, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The stem bark of Ailanthus altissima is used in traditional medicine in Asia to treat a variety of diseases, including cancer. The aim of this study was to identify compounds with tumoricidal activity from A. altissima stem bark and to investigate their mechanisms of action. Among the 13 compounds isolated from the ethyl acetate fraction of A. altissima stem bark, the ß-carboline alkaloid 9-hydroxycanthin-6-one had potent cytotoxicity in all three ovarian cancer cell types examined. 9-Hydroxycanthin-6-one induced apoptosis through the activation of caspases-3, -8, and -9. 9-Hydroxycanthin-6-one increased the intracellular levels of reactive oxygen species (ROS), and pre-treatment with the antioxidant N-acetyl-l-cysteine (NAC) attenuated the pro-apoptotic activity of 9-hydroxycanthin-6-one. Additionally, 9-hydroxycanthin-6-one was found to decrease the expressions of MCP-1 and RANTES, major determinants of macrophage recruitment at tumor sites, in ovarian cancer cells. Treatment with 9-hydroxycanthin-6-one inhibited the levels of M2 phenotype markers and some cancer-promoting factors, such as MMP-2, MMP-9, and VEGF, in macrophages educated in ovarian cancer conditioned medium. Taken together, these data suggest that 9-hydroxycanthin-6-one isolated from A. altissima stem bark induces apoptosis in human ovarian cancer cells through the caspase- and ROS-dependent pathways and inhibits the activation of tumor-associated macrophages.
[Mh] Termos MeSH primário: Ailanthus/química
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Alcaloides de Indol/farmacologia
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Ailanthus/metabolismo
Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/isolamento & purificação
Antioxidantes/farmacologia
Inibidores de Caspase/farmacologia
Caspases/química
Caspases/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Quimiocinas/genética
Quimiocinas/metabolismo
Feminino
Seres Humanos
Alcaloides de Indol/química
Alcaloides de Indol/isolamento & purificação
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Oligopeptídeos/farmacologia
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Casca de Planta/química
Casca de Planta/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (9-hydroxycanthin-6-one); 0 (Antineoplastic Agents, Phytogenic); 0 (Antioxidants); 0 (Caspase Inhibitors); 0 (Chemokines); 0 (Indole Alkaloids); 0 (Oligopeptides); 0 (Reactive Oxygen Species); 0 (Vascular Endothelial Growth Factor A); 0 (benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone); EC 3.4.22.- (Caspases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); WYQ7N0BPYC (Acetylcysteine)
[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:171212
[St] Status:MEDLINE



página 1 de 1270 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