Abstract
The inhibition of specific flavonoid on the in vitro platelet aggregation induced by collagen, arachidonic acid and thromboxane A2 (TxA2) agonist, seems to be related mostly to their ability to compete for binding to the TxA2 receptor (TP). The aim of this study was to analyze the effect of soy isoflavone and equol in terms of inhibiting the platelet aggregation and sCD40L release stimulated by ristocetin, an in vitro-activator of glycoprotein Ib/IX/V, in platelets from postmenopausal women. When platelets were stimulated by 0.75 mg/ml ristocetin, equol (10 μM) exhibited a greater inhibitory activity on platelet aggregation (~68%) than genistein or daidzein. The effect of equol was dependent on the concentration of platelet aggregation agonist. In the presence of ristocetin (0.75 mg/ml, 1.125 mg/ml and 1.5 mg/ml), the inhibitory effect of 10 μM equol was 68% ± 5%, 54% ± 4% and 31% ± 5%, respectively. Equol (10 μM) was a potent inhibitor (~35%) of sCD40L release when stimulated with 1.5 mg/ml ristocetin. However, no significant differences were noted in platelets incubated in the presence of genistein or daidzein and stimulated by ristocetin. On the other hand, SQ29548, a high TP antagonist, also inhibited the sCD40L release stimulated by ristocetin. Finally, 10 μM of genistein, daidzein or equol did not significantly affect the thromboxane B2 production when platelets were incubated with 1.5 mg/ml ristocetin. The relevance of this study was to find that equol exhibits a potent activity by inhibiting ristocetin-induced sCD40L release, suggesting that soy isoflavone has important biological effects on the hemostatic system. However, clinical trials will be necessary to assess the effect of equol on platelet and their impact on inflammatory markers.
Highlights
The bean of soy produces isoflavones, principally, genistein, daidzein and glycitein
We first tested the inhibitory capacity of genistein, daidzein and equol (10 μM) on platelets aggregation induced by 0.75 mg/ml ristocetin
The half maximal inhibitory concentration of equol for platelet aggregation stimulated by 0.75 mg/ml ristocetin, was approximately 8 μM (Figure 2)
Summary
The bean of soy produces isoflavones, principally, genistein, daidzein and glycitein. Isoflavones have been suggested as the principal chemical constituents responsible for the potential preventive effect of soy bean against risk factor of hormonerelated diseases and cardiovascular disease (CVD) [1] [2]. Different mechanisms have been proposed for the activity of isoflavones against risk factor of CVD, including estrogen-like effects, prevention of oxidative LDL and anti-platelets aggregation [3] [4]. Platelets initially interact with the sub endothelium via adhesive receptors such as glycoprotein Ib/IX/V receptors, which mediate rolling and tethering of the platelets to von Willebrand factor on the sites of vascular injury and induce glycoprotein IIb/IIIa activation, resulting in platelet aggregation [5]. We and other groups have shown that soy isoflavone compete for binding to TP in human platelets [10] [11]
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