Abstract
R-/S-2-(2-Hydroxypropanamido) benzoic acid (R-/S-HPABA), a marine-derived anti-inflammatory drug, however, the antiplatelet and antithrombotic effects have not been investigated. In this paper, the in vitro antiplatelet activities and in vivo antithrombotic effects of R-/S-HPABA were investigated, for the first time. The effects of R-/S-HPABA on platelet aggregation induced by adenosine diphosphate (ADP), collagen (COLL) and arachidonic acid (AA) were evaluated. In addition, the in vivo bleeding time, clotting time, collagen-epinephrine induced pulmonary thrombosis and common carotid artery thrombosis were also investigated in rats. R-/S-HPABA significantly inhibited ADP, COLL and AA induced platelet aggregation in rabbit platelet rich plasma in vitro compared with control group, to a degree similar to that of aspirin. Besides, R-/S-HPABA prolonged bleeding time and clotting time as well as increased the recovery rate obviously in pulmonary thrombosis. Moreover, the level of thromboxane B2 (TXB2) was decreased while the production of 6-keto-prostaglandin F1α (6-keto-PGF1α) was increased markedly by R-/S-HPABA. Furthermore, R-/S-HPABA reduced carotid artery thrombosis weight. These results illustrated that R-/S-HPABA could be a potent antiplatelet aggregation and antithrombotic agent.
Highlights
Thrombosis is that the blood form clots accompanied by insoluble fibrin and deposition of platelets on spalling or repaired surface of the cardiovascular system [1,2,3]
R-/S-HPABA could significantly inhibit the platelet aggregation induced by adenosine diphosphate (ADP) (5 mmol/L), arachidonic acid (AA) (20 mmol/L) and COLL (1 mg/mL) compared with the control group (p < 0.05)
These results suggest that R-/S-HPABA has an effect on platelet aggregation, especially on ADPinduced platelet aggregation
Summary
Thrombosis is that the blood form clots accompanied by insoluble fibrin and deposition of platelets on spalling or repaired surface of the cardiovascular system [1,2,3]. Efficient clotting limits the loss of blood at an injury site, whereas inappropriate formation of thrombin in veins or arteries is a common cause of disability and death [4, 5]. To the best of our knowledge, platelets play a major part in normal hemostasis and in the pathogenesis of thrombosis. Platelet activation make significant effects on initiation of haemostasis, thrombosis and various cardiovascular and cerebrovascular diseases [11, 12]. It is imperative to control platelets function in preventing and treating thrombosis events [13].
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