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Br J Nutr ; 89(5): 607-16, 2003 May.
Artigo em Inglês | MEDLINE | ID: mdl-12720581

RESUMO

There has been much recent interest in the cardiovascular benefits of dietary isoflavones. The aim of the present in vitro studies was to investigate potential anti-thrombogenic and anti-atherogenic effects of the isoflavones genistein and daidzein in platelets, macrophages and endothelial cells. Pre-treatment with either isoflavone inhibited collagen-induced platelet aggregation in a dose-dependent manner. In a macrophage cell line (RAW 264.7) activated with interferon gamma plus lipopolysaccharide, both isoflavones were found to inhibit NO production and tumour necrosis factor alpha (TNF-alpha) secretion dose-dependently, but they did not affect mRNA levels for inducible nitric oxide synthase and cyclo-oxygenase-2. Both isoflavones also dose-dependently decreased monocyte chemoattractant protein-1 secretion induced by TNF-alpha in human umbilical vein endothelial cells. Compared with daidzein, genistein exerted greater inhibitory effects for all parameters studied. The present data contributes to our knowledge on the molecular mechanisms by which isoflavones may protect against coronary artery disease. Further studies are required to determine whether the effects of isoflavones observed in the current in vitro studies are relevant to the aetiology of coronary artery disease in vivo.


Assuntos
Arteriosclerose/prevenção & controle , Endotélio Vascular/efeitos dos fármacos , Genisteína/farmacologia , Isoflavonas/farmacologia , Macrófagos/efeitos dos fármacos , Agregação Plaquetária/efeitos dos fármacos , Análise de Variância , Animais , Arteriosclerose/metabolismo , Linhagem Celular , Células Cultivadas , Quimiocina CCL2/metabolismo , Ciclo-Oxigenase 2 , Relação Dose-Resposta a Droga , Endotélio Vascular/metabolismo , Humanos , Isoenzimas/metabolismo , Ativação de Macrófagos , Macrófagos/metabolismo , Proteínas de Membrana , Camundongos , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase/metabolismo , Óxido Nítrico Sintase Tipo II , Prostaglandina-Endoperóxido Sintases/metabolismo , Fator de Necrose Tumoral alfa/biossíntese , Fator de Necrose Tumoral alfa/farmacologia
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