AI Article Synopsis
- Four specific ginsenosides were isolated from a newly processed ginseng and tested for their effects on platelet aggregation induced by various agents.
- Ginsenosides Rk1 and Rg5 strongly inhibited platelet aggregation caused by arachidonic acid, proving to be significantly more effective than acetylsalicylic acid (ASA), a known antiplatelet medication.
- Ginsenosides 20(S)-Rg3 and 20(R)-Rg3 exhibited only mild inhibitory effects on platelet aggregation compared to Rk1 and Rg5.
Article Abstract
Four dammarane glycosides, namely ginsenosides Rk1 (1), Rg5 (2), 20(S)-Rg3 (3), and 20(R)-Rg3 (4), isolated from a new processed ginseng, were evaluated for their inhibitory activity against platelet aggregation induced by adenosine diphosphate (ADP), collagen, arachidonic acid (AA) and U46619 (thromboxane A2 mimetic agent). Ginsenoside Rk1 and Rg5 inhibited AA-induced platelet aggregation in a dose dependent manner. Their activity against AA-induced platelet aggregation were found to be 8-22 fold higher than that of a known antiplatelet drug acetylsalicylic acid (ASA). They also inhibited U46619-induced platelet aggregation. Ginsenoside 20(S)-Rg3 and 20(R)-Rg3 showed mild inhibitory activity against AA and U46619-induced aggregation.
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