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KMID : 0352720130370020176
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Journal of Ginseng Research
2013 Volume.37 No. 2 p.176 ~ p.186
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Inhibitory effects of total saponin from Korean red ginseng via vasodilator-stimulated phosphoprotein-Ser157 phosphorylation on thrombin-induced platelet aggregation
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Lee Dong-Ha
Cho Hyun-Jeong
Kim Hyun-Hong
Rhee Man-Hee
Ryu Jin-Hyeob
Park Hwa-Jin
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Abstract
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In this study, we have investigated the effects of total saponin from Korean red ginseng (TSKRG) on thrombin-induced
platelet aggregation. TSKRG dose-dependently inhibited thrombin-induced platelet aggregation with IC50 value of about 81.1 μg/mL. In addition, TSKRG dose-dependently decreased thrombin-elevated the level of cytosolic-free Ca2+ ([Ca2+]i
), one of aggregation-inducing molecules. Of two Ca2+-antagonistic cyclic nucleotides as aggregation-inhibiting molecules, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), TSKRG significantly dose-dependently elevated intracellular level of cAMP, but not cGMP. In addition, TSKRG dose-dependently inhibited thrombin-elevated adenosine triphosphate (ATP) release from platelets. These results suggest that the suppression of [Ca2+]i elevation, and of ATP release by TSKRG are associated with upregulation of cAMP. TSKRG elevated the phosphorylation of vasodilator-stimulated phosphoprotein (VASP)-Ser157, a cAMP-dependent protein kinase (A-kinase) substrate, but not the phosphorylation of VASP-Ser239, a cGMPdependent protein kinase substrate, in thrombin-activated platelets. We demonstrate that TSKRG involves in increase of cAMP level and subsequent elevation of VASP-Ser157 phosphorylation through A-kinase activation to inhibit [Ca2+]i mobilization and ATP release in thrombin-induced platelet aggregation. These results strongly indicate that TSKRG is a beneficial herbal substance elevating cAMP level in thrombin-platelet interaction, which may result in preventing of platelet aggregation-mediated thrombotic diseases.
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KEYWORD
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Panax ginseng, Cytosolic-free Ca2+, Cyclic adenosine monophosphate, Adenosine triphosphate release, Vasodilator-stimulated phosphoprotein,
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