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Br J Nutr ; 89(5): 607-16, 2003 May.
Article in English | MEDLINE | ID: mdl-12720581

ABSTRACT

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.


Subject(s)
Arteriosclerosis/prevention & control , Endothelium, Vascular/drug effects , Genistein/pharmacology , Isoflavones/pharmacology , Macrophages/drug effects , Platelet Aggregation/drug effects , Analysis of Variance , Animals , Arteriosclerosis/metabolism , Cell Line , Cells, Cultured , Chemokine CCL2/metabolism , Cyclooxygenase 2 , Dose-Response Relationship, Drug , Endothelium, Vascular/metabolism , Humans , Isoenzymes/metabolism , Macrophage Activation , Macrophages/metabolism , Membrane Proteins , Mice , Nitric Oxide/metabolism , Nitric Oxide Synthase/metabolism , Nitric Oxide Synthase Type II , Prostaglandin-Endoperoxide Synthases/metabolism , Tumor Necrosis Factor-alpha/biosynthesis , Tumor Necrosis Factor-alpha/pharmacology
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