Key result
Diisoeugenol inhibits platelet aggregation and ATP release by blocking thromboxane formation and phosphoinositide breakdown.
Why the study?
The mechanisms by which diisoeugenol inhibits platelet aggregation and related biochemical pathways were not fully elucidated.
Does diisoeugenol inhibit platelet aggregation and thromboxane formation in rabbit and human platelets?
Does diisoeugenol inhibit platelet aggregation and thromboxane formation in rabbit and human platelets?
Diisoeugenol exerts antiplatelet effects by inhibiting thromboxane formation and phosphoinositides breakdown.
Diisoeugenol inhibited the platelet aggregation and ATP release of rabbit platelets caused by ADP, arachidonic acid, platelet-activating factor (PAF), collagen and thrombin. Prolongation of the incubation time of platelets with diisoeugenol did not cause further inhibition and the aggregability of platelets could not be restored after washing. In human platelet-rich plasma, diisoeugenol inhibited the biphasic aggregation and ATP release induced by adrenaline and ADP in a concentration-dependent manner. Thromboxane B2 formation caused by arachidonic acid, collagen and thrombin was markedly inhibited by diisoeugenol in a concentration-dependent manner. Diisoeugenol also inhibited the formation of inositol monophosphate caused by collagen, PAF and thrombin. The cAMP level of washed platelets was not changed by diisoeugenol. It is concluded that the antiplatelet effect of diisoeugenol is due to the inhibition of thromboxane formation and phosphoinositides breakdown.
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Lin et al. (1994) studied this question. Diisoeugenol was evaluated on Platelet aggregation, ATP release, thromboxane B2 formation, and phosphoinositides breakdown. Diisoeugenol inhibited platelet aggregation and ATP release in rabbit and human platelets by inhibiting thromboxane formation and phosphoinositides breakdown.
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