Mechanism of antiplatelet aggregation of angelica dahurica extract in human platelets

Abstract

Angelica dahurica extract (ADE) has been shown to exhibit antiplatelet aggregation properties, which promise to be used as a therapeutic agent for circulatory disorder. The aim of the present study was to investigate the mechanism of ADE in antiplatelet aggregation in human platelets. The effect of ADE on human platelet aggregation induced by adenosine diphosphate (ADP, 40 µM) and collagen (20 µg/ml) were explored in vitro, and the potential mechanism such activity were investigated using western blot analysis. The result showed that ADE at the concentration of 0.1, 0.25, 0.5 and 1 mg/ml significantly inhibited ADP-induced platelet aggregation by 38.2±13.7% (p<0.05), 50.2±11.6% (p=0.01), 73.4±8.5% (p<0.001) and 79.8±7.4% (p<0.001), respectively when compare to vehicle control. ADE at the concentration of 0.5 and 1 mg/ml significantly activated the phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at Ser157 (6.7±2.3 and 8.3±2.2; p<0.05), more than those at Ser239 (3.0±1.4; p=0.054 and 5.1±1.5; p=0.054), respectively, suggesting that VASP phosphorylation could mediated mainly through cAMP/PKA pathway. ADE at concentration of 0.1, 0.25, 0.5 and 1 mg/ml significantly inhibited collagen-induced platelet aggregation by 52.8±1%, 60.6±8.9%, 84.3±2% and 85.8± 2.3% (p<0.001), respectively when compare to vehicle control. ADE did not decrease phosphorylation of Akt at Thr308. In conclusion, the mechanism of antiplatelet aggregation of ADE may include the increase of VASP phosphorylation and mediated through cAMP/PKA pathway.