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Pesquisa : E01.370.225.500.335 [Categoria DeCS]
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Id: lil-774461
Autor: Marañón Cardonne, Miriam; Pérez Font, Lena; Font Santos, Oneida; Moya Gómez, Amanda.
Título: Modelos y ensayos para el estudio de la angiogénesis / Models and trials for angiogenesis study
Fonte: Medisan;20(1), ene.-ene. 2016.
Idioma: es.
Resumo: La angiogénesis, que conduce a la formación de redes capilares, tiene un rol importante en un elevado número de eventos fisiológicos y patológicos, entre los cuales figuran el desarrollo embrionario, la cicatrización de heridas, la artritis, el crecimiento tumoral, la metástasis y los procesos isquémicos, como uno de los mecanismos de la protección endógena y exógena. A tales efectos se analizan los métodos más utilizados actualmente tanto in vivo como in vitro para los estudios de angiogénesis; también se destacan las ventajas y desventajas de cada uno y se enfatiza en la combinación de ambos.

The angiogenesis that leads to the formation of capillary nets, has an important role in a high number of physiological and pathological events, among which we can mention the embryonic development, wounds healing, arthritis, tumoral growth, metastasis and in the ischemic processes as one of the mechanisms of the endogenous and exogenous protection. To such effects the most used methods at the moment are analyzed either in vivo or in vitro for the angiogenesis studies; advantages and disadvantages of each one are highlighted too and the combination of both is emphasized.
Descritores: Técnicas In Vitro
Neovascularização Fisiológica
Ensaio
Neovascularização Patológica
-Revisão
Ensaios de Migração Celular
Responsável: CU418.1 - Centro Provincial de Información de Ciencias Médicas de Santiago de Cuba


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Id: biblio-881862
Autor: Bellé, Luziane Potrich.
Título: Ação da proteína amiloide sérica A em melanomas / Activity of serum amyloid A protein in melanomas.
Fonte: São Paulo; s.n; 2015. 158 p. graf, tab, ilus.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Faculdade de Ciências Farmacêuticas para obtenção do grau de Doutor.
Resumo: Concentrações séricas basais da proteína amiloide sérica A (SAA) estão significativamente aumentadas em pacientes com câncer e alguns autores sugerem uma relação causal. Trabalho anterior do grupo mostrou que a SAA induz a proliferação de duas linhagens de glioblastoma humano e afeta os processos de invasividade in vitro, sustentando um papel pró-tumoral para esta proteína. Com base nesse trabalho, investigamos a abrangência dos efeitos de SAA para outro tipo de célula tumoral e para isso escolhemos um painel de linhagens de melanoma humano e uma linhagem primária obtida a partir de aspirado de linfonodo de paciente com melanoma, por nós isolada. Observamos que apesar da célula precursora de melanomas, isto é, melanócito, não produzir SAA, todas as linhagens de melanoma produziram a proteína e expressaram alguns dos seus receptores. Além disso, quando estas células foram estimuladas com SAA houve uma inibição da proliferação em tempos curtos de exposição (48 horas) e efeitos citotóxicos após um tempo maior (7 dias). A SAA também afetou processos de invasividade e a produção das citocinas IL-6, IL-8 e TNF-α. Aos avaliarmos o efeito da SAA na interação das células de melanoma com células do sistema imune, vimos que a SAA ativou uma resposta imune anti-tumoral aumentando a expressão de moléculas co-estumolatórias, como CD69 e HLA-DR, e sua função citotóxica. Ainda, vimos que a produção de TNF-α, IFN-γ, IL-10, IL-1ß e IL-8 estimuladas por SAA podem contribuir com os efeitos desta. De forma geral estes resultados nos levam a crer que a SAA tem atividade anti-tumoral em melanomas. Finalizando, com base na importância do desenvolvimento da resistência às terapias atuais para o melanoma, observamos que em células resistentes ao PLX4032, um inibidor de BRAF, os efeitos imunomodulatórios induzidos pela SAA estão abolidos, possivelmente identificando um novo componente da resistência

Basal serum concentrations of the protein serum amyloid A are significantly increased in cancer patients and some authors suggest a causal relationship. Previous work of our research group showed that SAA induces proliferation of two cell lines of human glioblastoma and affects invasiveness processes in vitro, supporting a pro-tumor role for this protein. Based on this work, we investigated the extent of SAA effects to another type of tumor cell and we chose a panel of human melanoma cell lines and primary line obtained from a patient with melanoma by lymph node aspirate. Melanoma cells were isolated by us. We observed that while the precursor cells of melanoma, melanocytes, do not produce SAA, all melanoma cell lines expressed the protein and produced some of their receptors. Moreover, when these cells were stimulated with SAA there was an inhibition of proliferation in short exposure times (48 hours) and cytotoxic effects after a longer period (7 days). SAA also affected invasive procedures and the production of the cytokines IL-6, IL-8 and TNF-α. To evaluate the SAA effect in the interaction of melanoma cells with immune system cells, we found that SAA activated an anti-tumor immune response by increasing the expression of co-estimulatory molecules such as CD69 and HLA-DR, and their cytotoxic function. Furthermore, we found that the production of TNF-α, IFN-γ, IL-10, IL-1ß and IL-8 stimulated by SAA can contribute to this effect. In general these results lead us to believe that the SAA has anti-tumor activity in melanomas. Finally, based on the importance of the resistance development to current therapies for melanoma we observed that in cells resistant to PLX4032, a BRAF inhibitor, the immunomodulatory effects induced by SAA are abolished, possibly identifying a new resistance component
Descritores: Melanoma/fisiopatologia
Proteína Amiloide A Sérica/efeitos adversos
Proteína Amiloide A Sérica/análise
-Ensaios de Migração Celular/instrumentação
Expressão Gênica
Proteínas Proto-Oncogênicas B-raf/efeitos adversos
Receptor para Produtos Finais de Glicação Avançada/genética
Receptor 2 Toll-Like/genética
Receptor 4 Toll-Like/genética
Responsável: BR40.1 - DBD - Divisão de Biblioteca e Documentacão do Conjunto das Químicas
BR40.1; T 616.0756, B438a. 30100022096-F


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Id: biblio-828173
Autor: Guo, C; Huang, T; Chen, A; Chen, X; Wang, L; Shen, F; Gu, X.
Título: Glucagon-like peptide 1 improves insulin resistance in vitro through anti-inflammation of macrophages
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;49(12):e5826, 2016. graf.
Idioma: en.
Projeto: National Science Foundation; . Zhejiang Provincial Natural Science Foundation.
Resumo: Glucagon-like peptide 1 (GLP-1), a kind of gut hormone, is used in the treatment of type 2 diabetes (T2D). Emerging evidence indicates that GLP-1 has anti-inflammatory activity. Chronic inflammation in the adipose tissue of obese individuals is a cause of insulin resistance and T2D. We hypothesized that GLP-1 analogue therapy in patients with T2D could suppress the inflammatory response of macrophages, and therefore inhibit insulin resistance. Our results showed that GLP-1 agonist (exendin-4) not only attenuated macrophage infiltration, but also inhibited the macrophage secretion of inflammatory cytokines including TNF-β, IL-6, and IL-1β. Furthermore, we observed that lipopolysaccharide (LPS)-induced macrophage conditioned media could impair insulin-stimulated glucose uptake. This effect was compensated by treatment with the conditioned media from macrophages treated with the combination of LPS and exendin-4. It was also observed that exendin-4 directly inhibited the activation of NF-κB in macrophages. In conclusion, our results indicated that GLP-1 improved inflammatory macrophage-derived insulin resistance by inhibiting NF-κB pathway and secretion of inflammatory cytokines in macrophages. Furthermore, our observations suggested that the anti-inflammatory effect of GLP-1 on macrophages can contribute to GLP-1 analogue therapy of T2D.
Descritores: Peptídeo 1 Semelhante ao Glucagon/farmacologia
Mediadores da Inflamação/farmacologia
Inflamação/tratamento farmacológico
Resistência à Insulina
Macrófagos/efeitos dos fármacos
Peptídeos/farmacologia
Peçonhas/farmacologia
-Tecido Adiposo/metabolismo
Ensaios de Migração Celular
Inflamação/metabolismo
Macrófagos/metabolismo
Limites: Humanos
Animais
Camundongos
Responsável: BR1.1 - BIREME


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Id: lil-744278
Autor: Mota, Matheus Alves de Lima; Landim, José Saul Peixoto; Targino, Thiago Sousa Silva; Silva, Silvia Fernandes Ribeiro da; Silva, Sônia Leite da; Pereira, Márcio Roberto Pinho.
Título: Evaluation of the anti-inflammatory and analgesic effects of green tea (Camellia sinensis) in mice
Fonte: Acta cir. bras;30(4):242-246, 04/2015. graf.
Idioma: en.
Resumo: PURPOSE: To evaluate the anti-inflammatory and analgesic effects of green tea (Camellia sinensis) in mice. METHODS: The anti-inflammatory effect of alcoholic extracts of green tea (AE) was evaluated in a cell migration assay with four groups of six Swiss mice receiving 0.07g/Kg or 0.14g/Kg EA (treatment groups), saline (negative control) or 10mg/Kg indomethacin (positive control) by gavage. One hour later 300 µg carrageen an was administered intraperitoneally or subcutaneously. The analgesic effect was evaluated using four groups of six animals receiving 0.07g/Kg or 0.14g/Kg EA, saline or 10mg/Kg indomethacin subcutaneously, followed 30 minutes later by 1% acetic acid. RESULTS: When administered subcutaneously at either dose (0.07g/Kg and 0.14g/Kg), AE inhibited carrageenan-induced cell migration (p<0.05). However, when administered by gavage, only the latter (0.14 g/Kg) was efficient (p<0.05). AE at both doses (0.07g/Kg and 0.14g/Kg) inhibited abdominal contortions (p<0.05), but the effect was not dose-dependent. CONCLUSION: Green tea was shown to have analgesic and anti-inflammatory properties and may constitute a natural treatment option in chronic inflammatory disorders. .
Descritores: Analgésicos/uso terapêutico
Anti-Inflamatórios/uso terapêutico
Camellia sinensis/química
Fitoterapia/métodos
Extratos Vegetais/uso terapêutico
Chá/química
-Ensaios de Migração Celular
Catequina/uso terapêutico
Infusões Subcutâneas
Indometacina/uso terapêutico
Inflamação/tratamento farmacológico
Reprodutibilidade dos Testes
Fatores de Tempo
Resultado do Tratamento
Limites: Animais
Masculino
Camundongos
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: lil-684524
Autor: Brazilian Journal of Medical and Biological Research; Sheng, W.J.; Jiang, H.; Wu, D.L.; Zheng, J.H..
Título: Early responses of the STAT3 pathway to platinum drugs are associated with cisplatin resistance in epithelial ovarian cancer
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;46(8):650-658, ago. 2013. graf.
Idioma: en.
Projeto: the National Natural Science Foundation of China.
Resumo: Cisplatin resistance remains one of the major obstacles when treating epithelial ovarian cancer. Because oxaliplatin and nedaplatin are effective against cisplatin-resistant ovarian cancer in clinical trials and signal transducer and activator of transcription 3 (STAT3) is associated with cisplatin resistance, we investigated whether overcoming cisplatin resistance by oxaliplatin and nedaplatin was associated with the STAT3 pathway in ovarian cancer. Alamar blue, clonogenic, and wound healing assays, and Western blot analysis were used to compare the effects of platinum drugs in SKOV-3 cells. At an equitoxic dose, oxaliplatin and nedaplatin exhibited similar inhibitory effects on colony-forming ability and greater inhibition on cell motility than cisplatin in ovarian cancer. Early in the time course of drug administration, cisplatin increased the expression of pSTAT3 (Tyr705), STAT3α, VEGF, survivin, and Bcl-XL, while oxaliplatin and nedaplatin exhibited the opposite effects, and upregulated pSTAT3 (Ser727) and STAT3β. The STAT3 pathway responded early to platinum drugs associated with cisplatin resistance in epithelial ovarian cancer and provided a rationale for new therapeutic strategies to reverse cisplatin resistance.
Descritores: Antineoplásicos/administração & dosagem
Resistencia a Medicamentos Antineoplásicos/fisiologia
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
/metabolismo
STATABATTOIRS TRANSCRIPTION FACTOR/metabolismo
Transdução de Sinais/efeitos dos fármacos
-Proteínas Reguladoras de Apoptose/genética
Linhagem Celular Tumoral
Ensaios de Migração Celular/métodos
Proliferação de Células/efeitos dos fármacos
Cisplatino/administração & dosagem
Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Proteínas Inibidoras de Apoptose/genética
Compostos Organoplatínicos/administração & dosagem
Oxazinas/farmacologia
Fator A de Crescimento do Endotélio Vascular/genética
Xantenos/farmacologia
Proteína bcl-X/genética
Limites: Animais
Humanos
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-647793
Autor: Zhang, Bicheng; Zhang, Yafei; Yao, Guoqing; Gao, Juan; Yang, Bo; Zhao, Yong; Rao, Zhiguo; Gao, Jianfei.
Título: M2-polarized macrophages promote metastatic behavior of Lewis lung carcinoma cells by inducing vascular endothelial growth factor-C expression
Fonte: Clinics;67(8):901-906, Aug. 2012. ilus, graf.
Idioma: en.
Projeto: China. Natural Science Foundation of Hubei Province; . China. Youth Dawn Plan of Science and Technology in Wuhan.
Resumo: OBJECTIVES: Tumor-associated macrophages that generally exhibit an alternatively activated (M2) phenotype have been linked to tumor progression and metastasis. However, the role of M2-polarized macrophages in the growth and metastasis of lung adenocarcinoma remains enigmatic. The aim of this study was to explore the effect of M2 macrophages on the proliferation and migration of mouse Lewis lung carcinoma cells and tumor-induced lymphangiogenesis. METHODS: Trypan blue staining and the Transwell migration assay were performed to evaluate the effects of activated (M1 or M2) macrophages on the proliferation and migration of Lewis cells. Furthermore, vascular endothelial growth factor-C expression in Lewis cells and nitric oxide secretion from activated macrophages were detected during the co-culture assay. Following treatment with activated macrophages, lymphatic endothelial cells differentiated into capillary-like structures, and the induction of Lewis cell migration was assessed using a twodimensional Matrigel-based assay. RESULTS: In the co-culture Transwell system, the proliferation and migration of Lewis cells were promoted by M2 macrophages. Moreover, the co-culture significantly increased the expression of vascular endothelial growth factor-C by Lewis cells and reduced the secretion of nitric oxide from M2 macrophages, which subsequently led to the capillary morphogenesis of lymphatic endothelial cells. Interestingly, following co-culture with Lewis cells, the function of RAW264.7 cells was polarized toward that of the M2 macrophage phenotype. CONCLUSION: M2-polarized macrophages promoted the metastatic behavior of Lewis cells by inducing vascular endothelial growth factor-C expression. Thus, the interruption of signaling between M2 macrophages and Lewis cells may be considered to be a new therapeutic strategy.
Descritores: Carcinoma Pulmonar de Lewis/secundário
Neoplasias Pulmonares/patologia
Macrófagos/fisiologia
Fator C de Crescimento do Endotélio Vascular/metabolismo
-Linhagem Celular Tumoral
Ensaios de Migração Celular
Movimento Celular
Proliferação de Células
Carcinoma Pulmonar de Lewis/metabolismo
Células Endoteliais/patologia
Neoplasias Pulmonares/metabolismo
Linfangiogênese/fisiologia
Macrófagos/citologia
Fatores de Tempo
Fator C de Crescimento do Endotélio Vascular/fisiologia
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-595833
Autor: Cavalcanti, Bruno Neves; Rode, Sigmar de Mello; França, Cristiane Miranda; Marques, Márcia Martins.
Título: Pulp capping materials exert an effect on the secretion of IL-1β and IL-8 by migrating human neutrophils
Fonte: Braz. oral res;25(1):13-18, Jan.-Feb. 2011. ilus, graf.
Idioma: en.
Projeto: State of São Paulo Research Foundation.
Resumo: Pulp repair is a complex process whose mechanisms are not yet fully understood. The first immune cells to reach the damaged pulp are neutrophils that play an important role in releasing cytokines and in phagocytosis. The objective of this study was to analyze the effect of different pulp-capping materials on the secretion of interleukin-1 beta (IL-1β) and interleukin-8 (IL-8) by migrating human neutrophils. Neutrophils were obtained from the blood of three healthy donors. The experimental groups were calcium hydroxide [Ca(OH)2], an adhesive system (Single Bond), and mineral trioxide aggregate (MTA). Untreated cells were used as control. Transwell chambers were used in performing the assays to mimic an in vivo situation of neutrophil chemotaxis. The pulp-capping materials were placed in the lower chamber and the human neutrophils, in the upper chamber. The cells were counted and the culture medium was assayed using ELISA kits for detecting and quantifying IL-1β and IL8. The data were compared by ANOVA followed by Tukey's test (p < 0.05). The secretion of IL-8 was significantly higher in all groups in comparison to the control group (p < 0.05). The adhesive system group showed higher IL-8 than the MTA group (p < 0.05). The secretion of IL-1β was significantly greater only in the MTA group (p < 0.001). It was concluded that only MTA is able to improve the secretion of IL-1β, and all materials tested increased IL-8 secretion. These results combined with all the other biological advantages of MTA indicate that it could be considered the material of choice for dental pulp capping.
Descritores: Capeamento da Polpa Dentária
Polpa Dentária/efeitos dos fármacos
Interleucina-1beta
INTERLEUKIN-ABDOMINAL NEOPLASMS/ECRET
Neutrófilos/efeitos dos fármacos
-Análise de Variância
Compostos de Alumínio/farmacologia
Bis-Fenol A-Glicidil Metacrilato/farmacologia
Cimentos para Ossos/farmacologia
Ensaios de Migração Celular
Compostos de Cálcio/farmacologia
Hidróxido de Cálcio/farmacologia
Combinação de Medicamentos
Polpa Dentária/imunologia
Teste de Materiais
Neutrófilos
Óxidos/farmacologia
Silicatos/farmacologia
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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