【摘要】 目的探讨GPⅡb/Ⅲa拮抗剂RGDS和钙通道拮抗剂Nifedipine对ADP诱导的血小板GPⅡb/Ⅲa活化的影响。方法 GP II b/11I a特异性抗体PAC-1标记活化GP II b/11I a,流式细胞仪检测静息及ADP(5μmol/L)诱导的血小板PAC-1表达率。结果静息状态下的血小板PAC-1表达率为(0.80±0.85)%;在ADP(5μmol/L)激动下,PAC-1表达率为(77.27±9.47)%;RGDS以浓度依赖性的方式抑制PAC-1表达率,IC50值为206μmol/L;Nifedipine能以浓度依赖性的方式抑制PAC-1表达率,IC50值为178μmol/L;RGDS联合Nifedipine对PAC-1表达的联合抑制率为(60.15±16.35)%,二者的交互效应差异有统计学意义(P<0.05)。结论 GPIIb/IIIa受体拮抗剂RGDS和Ca2+拮抗剂Nifedipine均抑制ADP诱导的血小板GPIIb/IIIa活化,其抑制作用呈浓度依赖性,随拮抗剂浓度增加抑制作用增强;两者对血小板GPIIb/IIIa活化的抑制存在协同作用。更多还原

【Abstract】 Objective This study is to find out the effect of GPIIb/IIIa antagonist RGDS and calcium channel antagonist Nifedipine on platelet GPⅡb/Ⅲa activation. Methods GPⅡb/Ⅲa activation was determined by the expression of PAC-1, an antibody against activated GP Ⅱ b/Ⅲ a, expression of PAC-1 stimulated with ADP(5μmol/L) was analyzed by a flow cytometer. Results To the healthy platelets, PAC-1 expression rate was(0.80±0.85) %; PAC-1 expression rate was(77.27±9.47) % on platelets induced by ADP(5μmol/L). RGDS could inhibit PAC-1-expression in a dose-dependent manner, the concentration producing 50% inhibition rate(IC50) is 206μmol/L. Nifedipine could inhibit PAC-1-expression in a dose-dependent manner, the concentration producing 50% inhibition rate(IC50) is 178μmol/L; The combined inhibition rate of RGDS and Nifedipine on PAC-1 binding was(60.15± 16.35)%, the interaction between Nifedipine and RGDS to PAC-1 binding was significant(P<0.05), both could strengthen each other’s effect. Conclusion Both GPIIb/IIIa antagonist RGDS and Ca2+ antagonist Nifedipine could inhibit GPIIb/IIIa activation in a dose-dependent manner. The inhibition rate increases when the concentration of RGDS or Nifedipine becomes higher. Both could strengthen each other’s effect on inhibiting platelet aggregation.更多还原