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目的观察2-(α-羟基戊基)苯甲酸钾盐对大鼠血小板聚集及前列环素/血栓素A2和纤溶系统的影响。方法大鼠随机分为正常对照组、2-(α-羟基戊基)苯甲酸钾盐(1.3、3.9、12.9 mg·kg-1)给药组和噻氯匹定组。2-(α-羟基戊基)苯甲酸钾盐静脉给药30 min后,腹主动脉取血,血小板聚集仪检测血小板聚集率,流式细胞术测定血小板表面CD62p的表达,放免法检测大鼠血浆血栓素B2和6-酮-前列腺素F1α含量,酶联免疫分析法检测组织型纤溶酶原激活剂和纤溶酶原激活物抑制物1的含量。结果 2-(α-羟基戊基)苯甲酸钾盐在对抗二磷酸腺苷、胶原、花生四烯酸和凝血酶4种诱导剂引起的血小板聚集中,可显著的、剂量依赖性的抑制二磷酸腺苷诱导的大鼠血小板聚集,降低血小板表面CD62p的表达,增加大鼠血浆前列环素代谢物6-酮-前列腺素F1α含量,对血栓素A2代谢物血栓素B2无影响,2-(α-羟基戊基)苯甲酸钾盐还明显减少纤溶酶原激活物抑制物1含量,不影响血浆中组织型纤溶酶原激活剂的含量。结论 2-(α-羟基戊基)苯甲酸钾盐可明显抑制二磷酸腺苷诱导的血小板聚集和活化,升高前列环素/血栓素A2比值,增强纤溶系统活性。
Objective To investigate the effect of 2- (α-hydroxypentyl) benzoate on platelet aggregation and prostacyclin / thromboxame A2 and fibrinolysis in rats. Methods The rats were randomly divided into normal control group, 2- (α-hydroxypentyl) benzoate potassium salt (1.3, 3.9, 12.9 mg · kg -1) and ticlopidine group. 30 min after the intravenous administration of 2- (α-hydroxypentyl) benzoate, the abdominal aorta was taken for blood, the platelet aggregation was measured for the platelet aggregation rate, the expression of CD62p on the platelet surface was measured by flow cytometry, Plasma thromboxane B2 and 6-keto-PGF1α levels were detected by enzyme-linked immunosorbent assay. Tissue plasminogen activator and plasminogen activator inhibitor-1 were detected by ELISA. Results Potassium 2- (α-hydroxypentyl) benzoate showed significant and dose-dependent inhibitory effects on platelet aggregation induced by four inducers of adenosine diphosphate, collagen, arachidonic acid and thrombin Adenosine triphosphate (ADP) -induced platelet aggregation in rats, decreased the expression of CD62p on the platelet surface, increased the content of 6-keto-prostaglandin F1α, a metabolite of prostacyclin in rats, had no effect on thromboxane B2, a thromboxane A2 metabolite, 2- α-hydroxypentyl) benzoate potassium salt also significantly reduced plasminogen activator inhibitor 1 content, does not affect plasma levels of tissue-type plasminogen activator. Conclusion Potassium 2- (α-hydroxypentyl) benzoate can significantly inhibit ADP-induced platelet aggregation and activation, and increase prostacyclin / thromboxane A2 ratio and increase fibrinolytic activity.