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目的 观察穿心莲成分 API0 1 34 (API)抗血小板活化和聚集的机制。方法 建立高脂血症家兔动脉血栓形成模型。观察穿心莲成分 API0 1 34 (API)对闭塞性血栓形成时间 (OT)、血小板聚集、血液血小板活化因子 (PAF)含量、血小板内三磷酸肌醇 (IP3)含量和 IP3受体 (IP3R)表达的影响。结果 API能够显著延长 OT和抑制血小板聚集 ,降低血液 PAF和血小板内 IP3含量 ,抑制血小板内 IP3R蛋白的表达。API 5 0 mg/ kg的抑制作用明显强于 API 5 m g/ kg。结论 API具有较强的抗血小板聚集和抗血栓形成作用 ,API对血小板 PAF- IP3/ IP3R信号途径的抑制作用 ,是 API抗血小板活化和聚集的机制之一
Objective To observe the antiplatelet activation and aggregation mechanism of Andrographis paniculata API0 1 34 (API). Methods To establish a model of arterial thrombosis in hyperlipidemic rabbits. Observed the effect of Andrographis paniculata API0134 (API) on occlusive thrombus time (OT), platelet aggregation, blood platelet activating factor (PAF) content, intraplatelet inositol trisphosphate (IP3) content, and IP3 receptor (IP3R) expression influences. Results The API can significantly prolong OT and inhibit platelet aggregation, reduce blood PAF and platelet IP3 content, and inhibit the expression of IP3R protein in platelets. The inhibitory effect of API 50 mg/kg was significantly stronger than that of API 5 mg/kg. Conclusions API has strong antiplatelet aggregation and antithrombotic effects. The inhibitory effect of API on platelet PAF-IP3/IP3R signaling pathway is one of the mechanisms of API antiplatelet activation and aggregation.