OBJECTIVES: The drawback of bleeding caused by chronic antiplatelet therapy is persecuting patients with thrombotic diseases severely. Based on the dual-directional regulatory effect of Panax notoginseng on platelet, the present study focused on the effect of Notoginsenoside Ft1, a saponin with effect in promoting platelet aggregation. KEY FINDINGS: According to the present study, Notoginsenoside Ft1 cannot stimulate platelet aggregation independently. However, the effect in enhancing aggregation induced by thrombin, collagen and ADP is peaked at 5-10 μm. In addition, thrombin-induced activation of PLCγ2-IP3 /DAG-[Ca2+ ]/PKC-TXA2 signalling was potentiated by Notoginsenoside Ft1, as well. Furthermore, the mice tail bleeding time was shortened by administration of Notoginsenoside Ft1 significantly. And the bleeding time prolonged by aspirin was also restored by Ft1. CONCLUSIONS: The haemostatic effect of Notoginsenoside Ft1 was exerted through potentiation of PLCγ2-IP3 /DAG-[Ca2+ ]/PKC-TXA2 signalling pathway stimulated by other stimulators. Notoginsenoside Ft1 has the potential to be developed into supplements in antiplatelet therapy to prevent the drawback of bleeding.
OBJECTIVES: The drawback of bleeding caused by chronic antiplatelet therapy is persecuting patients with thrombotic diseases severely. Based on the dual-directional regulatory effect of Panax notoginseng on platelet, the present study focused on the effect of NotoginsenosideFt1, a saponin with effect in promoting platelet aggregation. KEY FINDINGS: According to the present study, NotoginsenosideFt1 cannot stimulate platelet aggregation independently. However, the effect in enhancing aggregation induced by thrombin, collagen and ADP is peaked at 5-10 μm. In addition, thrombin-induced activation of PLCγ2-IP3 /DAG-[Ca2+ ]/PKC-TXA2 signalling was potentiated by NotoginsenosideFt1, as well. Furthermore, the mice tail bleeding time was shortened by administration of NotoginsenosideFt1 significantly. And the bleeding time prolonged by aspirin was also restored by Ft1. CONCLUSIONS: The haemostatic effect of NotoginsenosideFt1 was exerted through potentiation of PLCγ2-IP3 /DAG-[Ca2+ ]/PKC-TXA2 signalling pathway stimulated by other stimulators. NotoginsenosideFt1 has the potential to be developed into supplements in antiplatelet therapy to prevent the drawback of bleeding.