Impact Of GP Ⅱb/Ⅲa Receptor Antagonist On Platelet Releasing PMPs And Secreting VEGF And TXA₂

Objective:To investigate platelet glycoprotein GPⅡb/Ⅲa receptor antagonist (tirofiban) on platelet microparticle formation and vascular endothelial growth factor (VEGF), thromboxane A2(TXA2) release and the possible pathway to provide possible ways and bases for the cardiovascular diseases antiplatelet therapy efficacy observed.Methods:Eighteen cases of healthy adults, mean age26±4years old, all male, extract the antecubital venous blood,3.2%sodium citrate anticoagulant, the same cases of venous blood samples with different concentrations of tirofiban was (0ng/mL,50ng/mL,100ng/mL,300ng/mL, and500ng/mL), to intervene. Extract platelet rich plasma(PRP), the platelet was activated by10μM the ADP. Added the CD61-FITC, CD42a-PE fluorescent antibodies to mark the platelet microparticle(PMPs) and platelet, then analyzed platelet microparticle formation by flow cytometry. The platelet-rich plasma was frozed. Detected vascular endothelial growth factor (VEGF) and thromboxane A2(TXA2) via enzyme-linked immunosorbent assay.Results:1. The PMPs ratio of18healthy in normal resting state was (1.452±0.413)%, PMPs ratio increased significantly(16.652±6.403)%after the platelet was activated by ADP, the difference of PMPs ratio in resting state and actication state was statistically significant(P<0.05).2. The PMPs ratio in Ong/mL group was significantly higher than that in50,100,300,500ng/mL intervention groups(P<0.05, respectively), and with the tirofiban intervention concentration increase was gradually declined.3. The VEGF release in Ong/mL group was significantly higher than that in50,100,300,500ng/mL intervention groups(P<0.05, respectively), and with the tirofiban intervention concentration increase was gradully declined.4. The TXA2release in0ng/mL group was significantly higher than that in50,100,300,500ng/mL intervention groups(P<0.05, respectively), and with the tirofiban intervention concentration increase was gradully declined.Conclusion:1. Tirofiban could inhibit ADP induced platelet activation through platelet GPⅡb/Ⅲa receper pathway.2. Tirofiban could inhibit VEGF and TXA2release accompanied platelet activation through platelet GPⅡb/Ⅲa receptor pathway, blocking those factors mediated adverse biological effect.