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The in vitro effect of cinnamic aldehyde, a main component of Cinnamomi Cortex, on platelet aggregation and arachidonic acid (AA) metabolism in human platelets was studied. Cinnamic aldehyde reduced platelet aggregation of both platelet rich plasma and washed platelets, dose-dependently. This compound also decreased the formation of the metabolites of AA such as thromboxane B2 (TXB2), 12-hydroxy heptadecatrienoic acid and 12-hydroxyeicosatetraenoic acid in collagen-stimulated washed platelets. The conversion of exogenous [14C]AA to cyclooxygenase metabolites or 12-lipoxygenase metabolite was not altered significantly by the addition of cinnamic aldehyde. On the other hand, collagen-induced release of [14C]AA and its metabolites from washed platelets prelabeled with [14C]AA was markedly reduced by the addition of cinnamic aldehyde. These results suggested that cinnamic aldehyde suppressed the release of AA from platelet membrane phospholipids and then reduced the formation of thromboxane A2. This inhibitory effect of cinnamic aldehyde on AA release and TXB2 formation may contribute to reduced platelet aggregation.

In vitro effect of cinnamic aldehyde, a main component of Cinnamomi Cortex, on human platelet aggregation and arachidonic acid metabolism.