Abstract
Intracellular Ca2+ ([Ca2+]i) induces platelet aggregation, and influences the activation of aggregation associated-molecules. The increased [Ca2+]i activates both the Ca2+/calmodulin-dependent phosphorylation of the myosin light chain and the diacylglycerol-dependent phosphorylation of pleckstrin to trigger granule secretion (i.e., dense body and α-granule) and platelet aggregation. This study was carried out to elucidate the antagonistic effect of 20(S)-ginsenoside Rg3 (G-Rg3) present in Panax ginseng Mayer on Ca2+. G-Rg3 inhibited thrombin-induced human platelet aggregation in a dose-dependent manner and suppressed thrombin-induced elevation of [Ca2+]i mobilization. G-Rg3 increased the levels of cAMP, and subsequently, elevated the phosphorylation of inositol 1,4,5-triphosphate receptor I (Ser1756) during thrombin-induced human platelet aggregation. Moreover, G-Rg3 inhibited thapsigargin-induced Ca2+ influx and the thrombin-induced elevation of extracellular signal-regulated kinase 2 phosphorylation. G-Rg3 exhibited an inhibitory effect on [Ca2+]i levels leading to granule release and thus a therapeutic potential against platelet-mediated thrombotic disease is suggested.