氯吡格雷抑制急性冠状动脉综合征患者血小板释放可溶性CD40配体

Inhibitory effect of clopidogrel on release of soluble CD40 ligand from ADP-activated platelets in patients with non-ST-segment elevation acute coronary syndrome

目的探讨在非ST段抬高急性冠状动脉综合征(non-ST-segment elevation acute coronary syndromes,NSTEACS)患者短期应用氯吡格雷是否有抑制ADP诱导血小板释放可溶性CD40配体(sCD40L)的作用。方法NSTEACS42例,患者服用氯吡格雷6～8d,治疗前后采静脉血,提取富含血小板血浆(platelet rich plasma,PRP)并用二磷腺苷诱导血小板聚集和释放sCD40L,在不同时间点终止反应,用酶联免疫法测量sCD40L浓度,进行自身前后对照。结果治疗前后血浆sCD40L分别为(0.20±0.16)μg/L和(0.19±0.18)μg/L(P>0.05);治疗前后PRP受ADP诱导后20min释放的sCD40L浓度分别为(4.3±2.5)μg/L和(2.8±1.9)μg/L(P<0.001),诱导后40min释放的sCD40L浓度分别为(5.3±3.1)μg/L和(2.9±1.6)μg/L(P<0.001)。结论短期应用氯吡格雷可能对非ST段抬高急性冠状动脉综合征患者血小板炎症因子sCD40L释放具有抑制作用,提示氯吡格雷很可能具有抗炎效应。

Objectives To investigate the inhibitory effect of clopidogrel on release of soluble CD40 ligand （sCD40L） from ADP-activated platelets in patients with non-ST-segment elevation acute coronary syndromes （NSTEACS）. Methods Forty-two patients with NSTEACS were treated with clopidogrel for 6-8 days. The venous blood was drawn before and after treatment, respectively, to obtain platelet rich plasma （PRP） samples. The platelets were activated by adenosine diphosphate （ADP） , thus releasing sCD40L. And sCDdOL levels were determined by enzyme-linked immunosorbent assay （ELISA）. Results The plasma sCD40L concentration was （0.20 ± 0.16）μg/L before treatment and was （0.19 ± 0.18） μg/L after treatment （P〉 0.05）. Before treatment, the PRP sCD40L level at 20 minute of platelet activation was （4.3 ± 2.5）μg/L, and after treatment it deceased to （2.8 ± 1.9） μg/L （P〈0.001）. The corresponding levels at 40 minute of platelet activation were （5.3 ±3.1）μg/L and （2.9 ±1.6）μg/L, respectively （P〈0.001）. Conclusions Short-term clopidogrel administration inhibits the release of sCD40L from ADP-activated platelets in patients with NSTEACS, suggesting that, in addition to its antiplatelet potency, clopidogrel have an anti-inflammatory effect.