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桂皮醛对啮齿动物血小板聚集和血栓形成的抑制作用

Cinnamaldehyde reduction of platelet aggregation and thrombosis in rodents.

作者信息

Huang Jingqun, Wang Siwang, Luo Xiaoxing, Xie Yanhua, Shi Xinyou

机构信息

Institute of Materia Medica, School of pharmacy, Fourth Military Medical University, 17 Changlexi Street, Xi'an 710032, China.

出版信息

Thromb Res. 2007;119(3):337-42. doi: 10.1016/j.thromres.2006.03.001. Epub 2006 Apr 19.

DOI:10.1016/j.thromres.2006.03.001
PMID:16626787
Abstract

INTRODUCTION

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.

MATERIALS AND METHODS

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.

RESULTS

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).

CONCLUSIONS

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.

摘要

引言

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。

材料与方法

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。

结果

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。

结论

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。

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