Acetylsalicylic acid is compounding to antiplatelet effect of C-reactive protein

Abstract

The contribution of inflammatory process to the modulation of platelet response to acetylsalicylic acid (ASA) remains obscure. In our study, we examined the in vitro effect of C-reactive protein (CRP) on the ASA-mediated inhibition of collagen-stimulated platelet reactivity. Influence of CRP on platelet responsiveness to ASA was analysed using classical turbidimetric aggregation and flow cytometry. When acting alone, both C-reactive protein and ASA inhibited collagen-dependent platelet aggregation and reduced the expressions of two platelet surface membrane activation markers: P-selectin and activated GPIIbIIIa complex. Compared to the effects observed for ASA alone, the simultaneous action of both agents lead to further reductions in platelet aggregation (by 56.7 ± 1.0% vs. 14.9 ± 0.6%, p < 0.0001) and lowered the expressions of platelet surface membrane P-selectin (by 72.1 ± 5.3% vs. 65.0 ± 6.0%, p < 0.01) and activated GPIIbIIIa (by 67.0 ± 5.6% vs. 47.7 ± 8.3%, p < 0.01). In general, our findings showed for the first time the augmenting effect of native C-reactive protein in the antiplatelet action of acetylsalicylic acid. Thus, we conclude that the effectiveness of aspirin therapy may strongly depend upon the presence of native CRP in circulation.