Park H J, Rhee M H, Park K M, Nam K Y, Park K H
Department of Biochemical Pharmacology, Korea Ginseng and Tobacco Research Institute, Taejon.
J Ethnopharmacol. 1995 Dec 15;49(3):157-62. doi: 10.1016/0378-8741(95)01317-2.
The non-saponin fraction (NSF; lipophilic fraction) from the roots of Panax ginseng inhibited the aggregation of human platelets induced by thrombin (0.1 units/ml) in a dose-dependent manner. NSF induced the elevation of cGMP concentration in human platelets in a similar manner to molsidomine, a known vasodilator. NSF also inhibited Ca(2+)-influx into platelets. While verapamil, a Ca(2+)-antagonist, increased the cAMP level in platelets stimulated by thrombin, NSF had little effect on cAMP formation. Instead, NSF potently inhibited the thromboxane A2 (TXA2) production. The results suggest that NSF may regulate the levels of cGMP and TXA2 to inhibit platelet aggregation induced by thrombin.
人参根中的非皂苷部分(NSF;亲脂性部分)以剂量依赖性方式抑制凝血酶(0.1单位/毫升)诱导的人血小板聚集。NSF以与已知血管扩张剂吗多明类似的方式诱导人血小板中cGMP浓度升高。NSF还抑制Ca(2+)流入血小板。虽然钙拮抗剂维拉帕米可增加凝血酶刺激的血小板中的cAMP水平,但NSF对cAMP形成几乎没有影响。相反,NSF强烈抑制血栓素A2(TXA2)的产生。结果表明,NSF可能通过调节cGMP和TXA2水平来抑制凝血酶诱导的血小板聚集。