Mechanisms involved in the antiplatelet effect of C-phycocyanin

Abstract

C-phycocyanin (cpc), a biliprotein isolated fromSpirulina platensis, has been reported to exert many therapeutic and nutritional values. In the present study, we examined whether cpc has an antiplatelet activityin vitroand further investigated the possible anti-aggregatory mechanisms involved. Our results showed that preincubation of cpc (1–50μg/ml) with rabbit washed platelets dose-dependently inhibited the platelet aggregation induced by collagen (10μg/ml) or arachidonic acid (100μm), with an ic50of about 10μg/ml. Furthermore, the thromboxane B2formation caused by collagen or arachidonic acid was significantly inhibited by cpc due to suppression of cyclooxygenase and thromboxane synthase activity. Similarly, the rise of platelet intracellular calcium level stimulated by arachidonic acid and collagen-induced platelet membrane surface glycoprotein IIb/IIIa expression were also attenuated by cpc. In addition, cpc itself significantly increased the platelet membrane fluidity and the cyclic AMP level through inhibiting cyclic AMP phosphodiesterase activity. These findings strongly demonstrate that cpc is an inhibitor of platelet aggregation, which may be associated with mechanisms including inhibition of thromboxane A2formation, intracellular calcium mobilization and platelet surface glycoprotein IIb/IIIa expression accompanied by increasing cyclic AMP formation and platelet membrane fluidity.