Background: Glycoprotein IIb/IIIa (αIIb/β) is involved in platelet adhesion, and triggers a series of intracellular signaling cascades, leading to platelet shape change, granule secretion, and clot retraction. In this study, we evaluated the effect of ginsenoside Ro (G-Ro) on the binding of fibrinogen to αIIb/β.
Methods: We investigated the effect of G-Ro on regulation of signaling molecules affecting the binding of fibrinogen to αIIb/β, and its final reaction, clot retraction.
Results: We found that G-Ro dose-dependently inhibited thrombin-induced platelet aggregation and attenuated the binding of fibrinogen to αIIb/β by phosphorylating cyclic adenosine monophosphate (cAMP)-dependently vasodilator-stimulated phosphoprotein (VASP; Ser). In addition, G-Ro strongly abrogated the clot retraction reflecting the intensification of thrombus.
Conclusion: We demonstrate that G-Ro is a beneficial novel compound inhibiting αIIb/β-mediated fibrinogen binding, and may prevent platelet aggregation-mediated thrombotic disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5052406 | PMC |
| http://dx.doi.org/10.1016/j.jgr.2015.11.003 | DOI Listing |
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