CAJ | 학술논문

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。
목적：탐토GPⅡb/Ⅲa 길항제RGDS화개통도길항제Nifedipine대ADP유도적혈소판GPⅡb/Ⅲa활화적영향。방법GP II b／11I a특이성항체PAC-1표기활화GP II b／11I a，류식세포의검측정식급 ADP（5μmol/L)유도적혈소판PAC-1표체솔。결과정식상태하적혈소판PAC-1표체솔위(0.80±0.85)％；재ADP（5μmol/L）격동하，PAC-1표체솔위(77.27±9.47)%；RGDS이농도의뢰성적방식억제PAC-1표체솔，IC50치위206μmol/L；Nifedipine능이농도의뢰성적방식억제PAC-1표체솔，IC50치위178μmol/L；RGDS연합Nifedipine대PAC-1표체적연합억제솔위（60.15±16.35）％，이자적교호효응차이유통계학의의（P<0.05）。결론GPIIb/IIIa수체길항제RGDS화Ca2+길항제Nifedipine균억제ADP유도적혈소판GPIIb/IIIa활화，기억제작용정농도의뢰성，수길항제농도증가억제작용증강；량자대혈소판GPIIb/IIIa활화적억제존재협동작용。
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 GPⅡb/Ⅲa, 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.