Acidic peptides enhanced genistein-dependent inhibition of human platelet aggregation: potential protective effect of digestible peptides plus genistein against atherosclerosis

The leading cause of death in the United States and European countries is coronary heart disease. We hypothesized that the ingestion of soy compounds may not only have beneficial effects on atherosclerotic risk by lowering lipid compounds, but also by reducing platelet aggregability. Therefore, we analyzed in vitro the influence of defined and digestible peptides, frequently found in glycinin and β-conglycinin as important proteins of soy bean, on platelet aggregation of 180 healthy volunteers with or without the isoflavone genistein by aggregometry and flow cytometry. (i) The predominating share of amino acids and acidic, neutral, and basic di- and tripeptides of up to 2 mmol/L did not modify platelet aggregation induced by collagen, adenosine diphosphate, epinephrine, or arachidonic acid. (ii) Genistein inhibited agonist-induced platelet aggregation dose dependently. (iii) In the presence of the acidic peptides glutamate-glutamate and aspartate-aspartate-aspartate (1 mmol/L each), genistein reduced collagen- and ADP-dependent platelet activation stronger than 250 μmol/L of this isoflavone alone. Other peptides were less effective (eg, glutamate-glutamate-glutamate) or ineffective (eg, asparagine-asparagine). (iv) Glutamate-glutamate-glutamate (1 nmol/L), glutamate-glutamate (1 μmol/L), and aspartate-aspartate-aspartate (1 μmol/L) enhanced the inhibition of genistein on platelet aggregation induced by arachidonic acid. Thus, the results of the present in vitro investigation allow the assumption that nutrition with specific compounds of soy—acidic peptides together with genistein—might protect against coronary atherosclerosis by attenuating platelet activity. In vivo studies are warranted to check this assumption.