Abstract
Licochalcones extracted from Glycyrrhiza inflata are known to have a variety of biological properties such as anti-inflammatory, anti-bacterial, and anti-tumor activities, but their action on platelet aggregation has not yet been reported. Therefore, in this study we investigated the effects of licochalcones on platelet aggregation. Collagen and U46619, a thromboxane A2 receptor agonist, caused rabbit platelet aggregation, which was reversed by pretreatment with licochalcones A, C and D in concentration-dependent manners. Among these compounds, licochalcone A caused the most potent inhibitory effect on collagen-induced platelet aggregation. However, the licochalcones showed marginal inhibitory effects on thrombin or ADP-induced platelet aggregation. In addition to rabbit platelets, licochalcone A attenuated collagen-induced aggregation in human platelets. Because licochalcone A also inhibited arachidonic acid-induced platelet aggregation and production of thromboxane A2 induced by collagen in intact platelets, we further examined the direct interaction of licochalcone A with cyclooxygenase (COX)-1. As expected, licochalcone A caused an inhibitory effect on both COX-1 and COX-2 in vitro. Regarding the effect of licochalcone A on COX-1 enzyme reaction kinetics, although licochalcone A showed a stronger inhibition of prostaglandin E2 synthesis induced by lower concentrations of arachidonic acid, Vmax values in the presence or absence of licochalcone A were comparable, suggesting that it competes with arachidonic acid at the same binding site on COX-1. These results suggest that licochalcones inhibit collagen-induced platelet aggregation accompanied by inhibition of COX-1 activity.
Highlights
Platelets play critical roles in homeostatic functions through their adhesion and aggregation characteristics
We examined the effects of licochalcones on rabbit platelets and human platelets, and demonstrated that licochalcones inhibited platelet aggregation induced by collagen at lower concentrations compared with that by U46619, and was accompanied by an interaction with COX-1
All licochalcones significantly inhibited U46619 (3 μM)- and collagen (3 μg/ml)-induced platelet aggregation in concentration-dependent manners, and collagen-induced platelet aggregation was impaired compared with that induced by U46619 (Fig 2)
Summary
Licochalcones were provided by Research Laboratory of Minophagen Pharmaceutical Co. Ltd. Prostaglandin (PG) E2, d4-PGE2, U46619, COX-1, COX-2 and TXB2 EIA Kit were purchased from Cayman Chemical Company (Ann Arbor, MI). Collagen (Collagenreagent Horm) was purchased from Nycomed Pharma GMBH (Marburg, Germany). Thrombin was purchased from Wako Pure Chemicals (Osaka, Japan). Arachidonic acid and ADP were purchased from Sigma-Aldrich (St. Louis, MO) or Cayman Chemical Company. All other chemicals used were of reagent grade or the highest quality available
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