The aim of this study was to systematically examine the inhibitory mechanisms of C-phycocyanin(C-PC), one of the major phycobiliproteins of
Spirulina platensis (a blue-green alga), in plateletactivation. In this study, C-PC concentration-dependently (0.5-10 nM) inhibited platelet aggregationstimulated by agonists. C-PC (4 and 8 nM) inhibited intracellular Ca
2+ mobilization and thromboxaneA
2 formation but not phosphoinositide breakdown stimulated by collagen (1
![](/images/entities/mgr.gif)
g/mL) in human platelets.In addition, C-PC (4 and 8 nM) markedly increased levels of cyclic GMP and cyclic GMP-inducedvasodilator-stimulated phosphoprotein (VASP) Ser
157 phosphorylation. Rapid phosphorylation of aplatelet protein of
Mw 47 000 (P47), a marker of protein kinase C activation, was triggered by phorbol-12,13-dibutyrate (150 nM). This phosphorylation was markedly inhibited by C-PC (4 and 8 nM). Inaddition, C-PC (4 and 8 nM) markedly reduced the electron spin resonance (ESR) signal intensity ofhydroxyl radicals in collagen (1
![](/images/entities/mgr.gif)
g/mL)-activated platelets. The present study reports on a novel andvery potent (in nanomolar concentrations) antiplatelet agent, C-PC, which is involved in the followinginhibitory pathways: (1) C-phycocyanin increases cyclic GMP/VASP Ser
157 phosphorylation andsubsequently inhibits protein kinase C activity, resulting in inhibition of both P47 phosphorylationand intracellular Ca
2+ mobilization, and (2) C-PC may inhibit free radicals (such as hydroxyl radicals)released from activated platelets, which ultimately inhibits platelet aggregation. These results st
ronglyindicate that C-PC appears to represent a novel and potential antiplatelet agent for treatment of arterialthromboembolism.Keywords: Blue-green alga; C-phycocyanin; thromboxane A
2; protein kinase C; cyclic GMP; vasodilator-stimulated phosphoprotein; hydroxyl radical