摘要
目的:探讨3,4′,5-三羟基芪-3-β-单-D-葡萄糖苷(polydatin,Pol)抑制血小板聚集与其使血管内皮释放前列环素作用间的关系.方法:Pol与培养的人脐静脉内皮细胞(VEC,酶消化法)孵育为内皮组,无VEC为对照组,移细胞培养液至兔血小板(洗涤法),测凝血酶诱聚后血小板聚集率(PAR,比浊法)及上清液6-酮-前列环素F_(1alpha)(6-keto-PGF_(1α)),血栓烷B_2(TXB_2)含量(放免法).结果:无VEC组Pol不减少PAR;VEC组0.41 mmol·L^(-1)10 minPAR减少(-10±10),6-keto-PGF_(1α)增加(108±30 ng·L^(-1))(各与蒸馏水组之2±12,54±20ng·L^(-1)比).结论:Pol抑制血小板聚集与其增加VEC前列环素释放有关.
AIM:To study the relationship between the inhibiting effect on platelet aggregation and the enhancing effect on epoprostenol (PGI2) released from vascular endothelium with 3,4' ,5 - trihydroxystibene - 3 - (3 - mono - D -glucoside (polydatin, Pol). METHODS: After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothe-lial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group. Reduction of platelet aggregation rates (PAR. turbidity method) and changes of 6-ketoprostaglandin F1a ( 6-keto-PGF10 ) and thromboxane B2(TXB2) (radioimmunoassay method) in the supernatant of the aggregated platelets induced by thrombin were scrutinized. RESULTS: PAR in the control group showed no reduction, whereas PAR reduction (-10±10) and 6-keto-PGF1a increase (108±30ng·L-1) in the VEC group treated 10min with Pol 0. 41 mmol·L-1 (vs that of distilled water, ie, 2+12 and 54±20 ng·L-1) occurred. CONCLUSION: Increase of PGI2 from VEC by Pol was involved in its (Pol' s) inhibition effect of platelet aggregation.
出处
《中国药理学报》
CSCD
1995年第3期265-268,共4页
Acta Pharmacologica Sinica
关键词
POL
葡萄糖苷
血管内皮
血小板聚集
前列环素
3,4',5-trihydroxystibene-3-β-mono-D-glucoside
polydatin
umbilical veins
vascular endothelium
platelet aggregation
thromboxane A_2
thromboxane B_2
epoprostenol
6-ketoprostaglandin F_(1alpha).