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Cepharanthine incorporated into rabbit platelets dose dependently, inhibited calcium influx as well as aggregation in response to collagen, and also inhibited arachidonate release in response to collagen and A23187 in the same concentration ranges. The latter action of cepharanthine was shown not to be due to the direct action on phospholipase A2 molecules but to the depression of susceptibility of substrate phospholipids to enzymatic hydrolysis. These depressed functions, as well as the inhibited aggregation, were almost restored by removing the bound drugs from the platelets. Arachidonate-induced aggregation and prostaglandin synthesis from externally added arachidonate were not suppressed by the addition of cepharanthine. These results suggest that cepharanthine physically changes the lipid properties and thereby inhibits the function of the calcium channel or the susceptibility of substrate phospholipids to enzymatic hydrolysis by phospholipase A2.
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