Inhibition of thromboxane formation as the antiplatelet mechanism of 3,4-dihydroxyxanthone and quercetin pentaacetate.

3,4-Dihydroxyxanthone and quercetin pentaacetate were shown to inhibit the aggregation and ATP release of washed rabbit platelets induced by collagen and arachidonic acid, but were not induced by PAF. This inhibition was reversible and in a concentration-dependent manner. The thromboxane B2 formation of washed rabbit platelets, which was caused by arachidonic acid and collagen, was also suppressed by both antiplatelet agents. In human platelet-rich plasma, 3,4-dihydroxyxanthone and quercetin pentaacetate inhibited the secondary, but not the primary aggregation induced by ADP and epinephrine. Both antiplatelet agents also inhibited collagen- and arachidonic acid-induced aggregation in whole blood in a dose-dependent manner. It is concluded that the antiplatelet effects of 3,4-dihydroxyxanthone and quercetin pentaacetate are due to the inhibition of thromboxane formation.