摘要
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 en- zyme-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 - 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 en- zyme-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.
