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. In order to obtain platelet rich plasma (PRP) samples, the venous blood was drawn before and after treatment, respectively. The platelets were activated by adenosine diphosphate (ADP), thus releasing sCD40L. sCD40L levels were determined by enzyme-linked immunosorbent assay (ELISA) at different time of the reaction. Results Plasma sCD40L concentration before treatment was (0.199±0.155) ng/mL, and (0.190±0.176) ng/mL after treatment (P>0.05). Before treatment the PRP sCD40L level at 20-minute of platelet activation was (4.34±2.51) ng/mL, and decreased to (2.79±1.93) ng/mL after treatment (P<0.001). The corresponding level at 40-minute of platelet activation was (5.29±3.13) ng/mL before treatment and (2.87±1.59) ng/mL after treatment(P<0.001). Conclusions Short-term clopidogrel administration might inhibit the release of sCD40L by ADP-activated platelet in patients with NSTEACS, suggesting that, in addition to its antiplatelet potency, clopidogrel may still have an anti-inflammatory effect. 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 to 8 days. In order to obtain platelet rich plasma (PRP) samples, the venous blood was drawn before and after treatment, respectively. The platelets were activated by adenosine diphosphate (ADP), which releases sCD40L. SCD40L levels were determined by enzyme Results Plasma sCD40L concentration before treatment was (0.199 ± 0.155) ng / mL, and (0.190 ± 0.176) ng / mL after treatment (P> 0.05). Before treatment the PRP sCD40L level at 20-minute of platelet activation was 4.34 ± 2.51 ng / mL and decreased to 2.79 ± 1.93 ng / mL after treatment (P <0.001). The corresponding level at 40-minute of platelet activation was (5.29 ± 3.13) ng / mL before treatm ent and (2.87 ± 1.59) ng / mL after treatment (P <0.001) Conclusions Short-term clopidogrel administration might inhibit the release of sCD40L by ADP-activated platelet in patients with NSTEACS, suggesting that, in addition to its antiplatelet potency, clopidogrel may still have an anti-inflammatory effect.