Ginsenoside Rk3 suppresses U46619-induced human platelets aggregation through regulation of cAMP and PI3K/Akt pathway

Proper activation and aggregation of platelets are necessary, but excessive or abnormal aggregation can lead to cardiovascular diseases such as stroke, thrombosis, and atherosclerosis.Therefore, identifying a substance that can regulate or inhibit platelet aggregation is important for preventing and treating these diseases.Several studies have shown that certain ginsenoside compounds in Panax ginseng can inhibit platelet aggregation.Among these compounds, Rk3 (G-Rk3) from Panax ginseng needs to be further explored in order to reveal the mechanisms of action during inhibition.G-Rk3 significantly increased amounts of cyclic adenosine monophosphate (cAMP) and led to significant phosphorylation of cAMP-dependent kinase substrates vasodilatorstimulated phosphoprotein and inositol 1,4,5-trisphosphate receptor.Furthermore, the effect of G-Rk3 extended to the inhibition of PI3K/Akt phosphorylation resulting in the reduced secretion of intracellular granules.Ultimately, G-Rk3 effectively inhibited platelet aggregation.Therefore, we suggest G-Rk3's potential as a prophylactic or therapeutic agent for cardiovascular diseases caused by faulty platelet aggregation.