银杏内酯B衍生物抗血小板聚集作用和作用机制(英文)

Antagonistic Effect and Mechanism of a New Derivative of Gingkolide B on Platelet Aggregation

目的:探讨银杏内酯B衍生物(XQ)抗血小板聚集的作用及其机制。方法:运用比浊法测定静脉给药后PAF诱导的家兔血小板聚集作用,采用放射配基结合试验观察[3H]PAF与兔血小板受体特异性结合的作用。结果:XQ1.95、3.90、7.80mg·kg-1对家兔血小板聚集的抑制率分别为29.8%、43.5%和55.2%(P<0.01),PAF与家兔血小板膜上PAF受体结合的平衡解离常数(KD)=8.31×10-5mmol·L-1,最大结合容量(BMAX)=2.62×10-9mmol/108血小板。XQ和银杏内酯B(GB)可抑制[3H]PAF与兔血小板受体的特异性结合,抑制常数(Ki)分别为8.72×10-8、7.13×10-7mol·L-1。结论:XQ具有抗血小板聚集作用,Ki值接近,其拮抗PAF受体的能力与GB相似。

AIM： To study antagonistic effect and mechanism of a new derivative of ginkolide B named XQ on platelet aggregation. METHODS： To assay inhibiting effect of XQ on PAF-induced platelet aggregation with turbidimetry method, rabbits were administered at different final concentrations via iv at different times. The specific binding of ^[3H]PAF to rabbit platelet receptor was investigated by radio ligand binding assay （RLBA）. RESULTS： Three groups （1.95, 3.9, 7.8 mg·kg^-1） had significant effect on inhibiting PAF-induced platelet aggregation in rabbits, and inhibition ratio were 29.8%, 43.5% and 55.2% respectively （compared to normal group, P〈0.01） The equilibrium dissociation constant （KD） and maximum binding capacity of ^[3H]PAF were 8.31×10^-5mmol·L^-1 and 2.62×10^-9mmol/10^8 platelets respectively. Something about XQ and GB＇s specific binding inhibition was found that the Ki of XQ and GB were 8.72×10^-8 and 7.13×10^-7mol·L^-1 respectively. CONCLUSION： XQ can inhibit platelet aggregation by competitively occupying specific PAF receptor site on blood platelet membrane.