Ginsenoside Ro (Polysciasaponin P3; Chikusetsusaponin 5; Chikusetsusaponin V) exhibits a Ca-antagonistic antiplatelet effect with an IC50 of 155 ?μM. Ginsenoside Ro reduces the production of TXA2 more than it reduces the activities of COX-1 and TXAS.
性状
Solid
IC50 & Target[1][2]
TXA2/TP TXA2
体外研究(In Vitro)
Ginsenoside Ro in Panax ginseng is a beneficial novel Ca-antagonistic compound and may prevent platelet aggregation-mediated thrombotic disease. Ginsenoside Ro dose-dependently reduces thrombin-stimulated platelet aggregation, and IC50 is approximately 155?μM. Ginsenoside Ro inhibits TXA2 production to abolish thrombin-induced platelet aggregation. Thromboxane A2 (TXA2) induces platelet aggregation and promotes thrombus formation. Ginsenoside Ro dose-dependently (50-300 μM) reduces the TXB2 level that is induced by thrombin; Ginsenoside Ro (300 μM) inhibits the thrombin-mediated elevation in TXB2 level by 94.9%. COX-1 activity in the absence of Ginsenoside Ro (negative control) is 2.3±0.1 nmol/mg protein. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, COX-1 activity
体内研究(In Vivo)
Ginsenoside Ro dissolved in water is administrated by gavage to mice at doses of 25 and 250?mg/kg/day for 4 days before i.v. injection of HT29 in order to keep blood concentrations of Ginsenoside Ro above a certain level before HT29 i.v. injection followed by 40 days of oral administration of Ginsenoside Ro to the mice. After 38 days of treatment, the animals are euthanized, and the number of pulmonary metastatic nodules is counted in addition to evaluation of toxicity of Ginsenoside Ro and mouse pathology by HT29. Ginsenoside Ro (250?mg/kg/day) produces a significant decrease in the number of tumor nodules on the lung surface, yielding inhibition rates of 88% (P?<?0.01).Medlife has not independently confirmed the accuracy of these methods. They are for reference only.