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

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．

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

Objectives To investigate the inhibitory effect of clopidogrel on release of soluble CD40 ligand (sCD40L) by ADP-activated platelet 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 sCD40L levels were determined by enzyme-linked immunosorbent assay (ELISA) at different time. Results The plasma sCD40L concentration before treatment was 1.99±1.55 ng/ml, and after treatment it was 1.90±1.76ng/ml (P>0.05). Before treatment the PRP sCD40L level at 20-minute of platelet activation was 4.34±2.51ng/ml, and after treatment it deceased to 2.79±1.93ng/ml (P<0.001). The corresponding levels at 40-minute of platelet activation were 5.29±3.13ng/ml and 2.87±1.59ng/ml, respectively (P<0.001). Conclusions Short-term clopidogrel administration might inhibit the release of soluble CD40 ligand by ADP-activated platelets in patients with non-ST-segment elevation acute coronary syndromes, suggesting that, in addition to its antiplatelet potency, clopidogrel may still have an anti-inflammatory effect.