癌胚抗原相关细胞黏附分子源性多肽KM17对血小板活化作用的研究

Effect of CEACAM1-derived peptide KM17 on platelet activation

摘要:

目的 探讨癌胚抗原相关细胞黏附分子（CEACAM1）源性多肽KM17对血小板聚集、释放、黏附功能的影响。方法 采用血小板聚集仪观察多肽KM17对凝血酶、胶原、花生四烯酸（AA）、二磷酸腺苷（ADP）等激动剂诱导的血小板聚集的影响；流式细胞术观察多肽KM17对ADP激活血小板后P-选择素释放的影响；显微镜下观察多肽KM17对血小板静态黏附于胶原基质的影响。结果 多肽KM17能显著促进ADP诱导的血小板聚集且呈剂量依赖（P <0.05），而对AA、胶原及凝血酶诱导的血小板聚集差异均无统计学意义（P >0.05）；此外，多肽KM17对ADP激活血小板后P-选择素释放及血小板静态黏附于胶原基质的差异也无统计学意义（P >0.05）。结论 多肽KM17可明显促进ADP诱导的血小板聚集，但对ADP活化血小板后P-选择素释放及血小板静态黏附于胶原基质未见明显作用。

Abstract:

Objective To explore the effect of KM17, a synthetic CEACAM1-derived peptide, on platelet aggregation, release, and adhesion.Methods We examined the effect of KM17 on platelet aggregation induced by different agonists (ADP, thrombin, collagen, and AA) with aggregometer. We observed the effect of KM17 on platelet P-selectin release after stimulated by ADP with FCM. The effect of KM17 on platelet adhesion to collagen was observed under a microscope.Results KM17 dose-dependently promoted ADP-induced platelet aggregation (P < 0.05), but had no significant effect on platelet aggregation induced by AA, collagen, and thrombin (P > 0.05). In addition, KM17 had no significant effect on platelet P-selectin release induced by ADP (P > 0.05), and there was no significant difference in the numbers of platelet adhesion to collagen after incubated with different concentrations of KM17 (P > 0.05).Conclusions KM17 dose-dependently promoted platelet aggregation induced by ADP, but had no significant effect on platelet P-selectin release induced by ADP, and on platelet adhesion to collagen.