摘要
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
Objective To observe the mechanism of API 0134 (API) against platelet activation and aggregation. Methods An arterial thrombosis model of rabbits with high cholesterolemia was established. The effects of API 0134 (API) on the occlusive thrombosis time (OT), platelet aggregation function, level of blood platelet activiting factor (PAF), content of inositol trisphosphate (IP 3 ) and expression of IP 3 receptor of platelets were observed. Results API could obviously prolong OT and inhibit platelet aggregation, decrease the level of blood PAF and the content of IP 3 of platelets, and markedly inhibit the expression of IP 3 R protein in API group as compared with thrombosis model group in a dose dependent manner. Conclusion API exerts a strong effects against platelet thrombosis and aggregation. The inhibitive effects of API on platelet PAF IP 3 /IP 3 R signaling pathway may be one of the mechanisms of API against platelet activation and aggregation.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2003年第2期149-151,共3页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目 (No. 39870 92 4 )
