Huang Jingqun, Wang Siwang, Luo Xiaoxing, Xie Yanhua, Shi Xinyou
Institute of Materia Medica, School of pharmacy, Fourth Military Medical University, 17 Changlexi Street, Xi'an 710032, China.
Thromb Res. 2007;119(3):337-42. doi: 10.1016/j.thromres.2006.03.001. Epub 2006 Apr 19.
Cinnamaldehyde (CA) has been reported to inhibit in vitro aggregation in human and rabbit platelets; however, little is known about the antithrombotic activities of CA in vivo.
We tested the effects of CA on collagen- or thrombin-induced aggregation of rat platelets in vitro. Hemorrhage and coagulation times of mice treated with CA by the tail-cutting or slide method were measured. We also tested the life-saving effects of CA on experimental models of thrombosis in mice and rats. The anti-platelet effects of CA were examined in rats.
CA inhibited collagen- and thrombin-induced platelet aggregation in vitro in a concentration-dependent manner. In mice, CA administration (250, 500 mg/kg orally and 50, 100 mg/kg i.p.) markedly prolonged hemorrhage and coagulation times and effectively reduced the mortality rate of collagen-epinephrine-induced acute pulmonary thromboembolism. In an arteriovenous shunt thrombosis rat model, the CA administration (250, 500 mg/kg orally and 50, 100 mg/kg i.p.) for 10 days dose-dependently decreased thrombus weight. Administration of CA also significantly inhibited collagen-induced platelet aggregation in the rat platelet-rich plasma (PRP).
The results demonstrate that CA may be a promising antithrombotic agent, and its antithrombotic activity may be due to anti-platelet aggregation activity in vitro and in vivo.
据报道,肉桂醛(CA)可抑制人和兔血小板的体外聚集;然而,关于CA在体内的抗血栓形成活性知之甚少。
我们测试了CA对大鼠血小板在体外由胶原蛋白或凝血酶诱导的聚集的影响。通过断尾或玻片法测量用CA处理的小鼠的出血时间和凝血时间。我们还测试了CA对小鼠和大鼠血栓形成实验模型的挽救生命的作用。在大鼠中研究了CA的抗血小板作用。
CA在体外以浓度依赖的方式抑制胶原蛋白和凝血酶诱导的血小板聚集。在小鼠中,给予CA(口服250、500mg/kg以及腹腔注射50、100mg/kg)显著延长出血时间和凝血时间,并有效降低胶原蛋白-肾上腺素诱导的急性肺血栓栓塞的死亡率。在动静脉分流血栓形成大鼠模型中,给予CA(口服250、500mg/kg以及腹腔注射50、100mg/kg)10天,血栓重量呈剂量依赖性降低。给予CA还显著抑制富含大鼠血小板血浆(PRP)中胶原蛋白诱导的血小板聚集。
结果表明,CA可能是一种有前景的抗血栓形成药物,其抗血栓形成活性可能归因于其在体外和体内的抗血小板聚集活性。