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目的:研究柯里拉京(Corilagin)的抗血栓形成作用及其机制。方法:运用电刺激大鼠颈动脉血栓形成模型评价corilagin对血栓形成的影响,采用Born方法测定血小板聚集功能的影响;应用玫瑰花结试验及Born方法分别探讨Corilagin对中性粒细胞与血小板间的相互作用。结果:10和20 mg.kg-1的corilagin均明显延长大鼠颈动脉的血栓形成时间。Corilagin呈浓度依赖性显著抑制ADP和血小板活化因子(PAF)诱导的血小板聚集,其半数抑制浓度(50%inhibitory concentration,IC50)分别为115.6和264.8μmol.L-1,对花生四烯酸(AA)诱导的血小板聚集无明显作用;Corilagin显著降低血小板与中性粒细胞之间的粘附率,其IC50为73.5μmol.L-1。Corilagin明显抑制肉豆蔻佛波醇(fMLP)激活的中性粒细胞上清液引起的血小板聚集,IC50为134.3μmol.L-1。结论:Corilagin呈剂量依赖性明显对抗血栓形成。其机制与其抑制血小板聚集和阻抑血小板与中性粒细胞之间相互作用密切相关。
Objective: To study the antithrombotic effects and mechanisms of Corilagin. METHODS: The effect of corilagin on thrombosis was assessed by electrical stimulation of rat carotid artery thrombosis model. Born assay was used to determine the effect of platelet aggregation. The effects of Corilagin on neutrophil and platelet were studied by rosette test and Born method. interaction. RESULTS: Corilagin at both 10 and 20 mg.kg-1 significantly prolonged thrombus formation in rat carotid arteries. Corilagin significantly inhibited platelet aggregation induced by ADP and platelet activating factor (PAF) in a concentration-dependent manner, and its half inhibitory concentration (IC50) was 115.6 and 264.8 μmol.L-1, respectively, for arachidonic acid (AA). Induced platelet aggregation had no significant effect; Corilagin significantly reduced the adhesion rate between platelets and neutrophils, and its IC50 was 73.5 μmol.L-1. Corilagin significantly inhibited platelet aggregation by neutrophil supernatant activated by fMLP, with an IC50 of 134.3 μmol.L-1. CONCLUSION: Corilagin is dose-dependently apparently resistant to thrombosis. Its mechanism is closely related to inhibiting platelet aggregation and inhibiting the interaction between platelets and neutrophils.