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| 穿心莲成分对血栓模型家兔血小板三磷酸肌醇及其受体表达的影响 | |
| 引用本文： | 王宏伟,李树生,王国平,陶德定,赵华月.穿心莲成分对血栓模型家兔血小板三磷酸肌醇及其受体表达的影响[J].华中科技大学学报(医学版),2003,32(2):149-151. |
| 作者姓名： | 王宏伟 李树生 王国平 陶德定 赵华月 |
| 作者单位： | 1. 华中科技大学同济医学院附属同济医院儿科,武汉,430030 2. 华中科技大学同济医学院基础医学院病理学系,武汉,430030 3. 华中科技大学同济医学院附属同济医院心内科,武汉,430030 |
| 基金项目： | 国家自然科学基金资助项目 (No. 39870 92 4 ) |
| 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 API抗血小板活化和聚集的机制之一 |
| 关 键 词： | 穿心莲 血小板活化 三磷酸肌醇 |
| 修稿时间： | 2002年2月27日 |
Effects of API0134 on IP3 and Expression of IP3 Receptor of Pl atelets in Rabbit Thrombosis Model |
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| Wang Hongwei ,Li Shusheng ,Wang Guoping et al.Effects of API0134 on IP3 and Expression of IP3 Receptor of Pl atelets in Rabbit Thrombosis Model[J].Journal of Huazhong University of Science and Technology(Health Sciences),2003,32(2):149-151. | |
| Authors: | Wang Hongwei Li Shusheng Wang Guoping |
| Institution: | Wang Hongwei 1,Li Shusheng 1,Wang Guoping 2 et al 1 Department of Pediatrics,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030 2 Department of Pathology,School of Basic Medical Sciences,Huazhong University of Science and Technology,Wuhan 430030 |
| Abstract: | 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. |
| Keywords: | andrographis paniculata nees platelet inositol trisphosphate |
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