检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:王宏伟[1] 李树生[2] 赵华月[3] 王国平[4]
机构地区:[1]华中科技大学同济医学院同济医院儿科,湖北省武汉市430030 [2]华中科技大学同济医学院同济医院急诊科,湖北省武汉市430030 [3]华中科技大学同济医学院同济医院心内科,湖北省武汉市430030 [4]华中科技大学同济医学院病理系,湖北省武汉市430030
出 处:《中国动脉硬化杂志》2002年第4期285-287,共3页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金 ( 39870 92 4)资助
摘 要:建立高脂血症家兔动脉血小板依赖性血栓模型 ,应用流式细胞术、放射免疫法及3 H 肌醇掺合等检测方法观察穿心莲成分API0 134对闭塞性血栓形成时间、血小板聚集功能、血小板胞浆游离Ca2 +和Mg2 +浓度以及血小板内环磷酸腺苷、环磷酸鸟苷和三磷酸肌醇含量的影响。结果发现 ,API0 134能够显著延长闭塞性血栓形成时间和抑制血小板聚集。 5 0mg kgAPI0 134的药理作用明显强于 5mg kgAPI0 134。API0 134可显著抑制血栓形成所诱导的血小板内 [Ca2 +]i、[Mg2 +]i和三磷酸肌醇浓度升高 ,显著抑制血小板内环磷酸腺苷浓度降低。抑制作用与用药剂量有关。结果提示 ,API0 134具有较强的抗血栓形成和抗血小板聚集作用。抗血小板聚集的作用机制与调节血小板信号转导物质 [Ca2 +]i、[Mg2 +]i。Aim To observe the effects of API0134 on arterial thrombus formation and exploring the mechanism of anti-platelet aggregation. Methods An thrombus model of rabbits with high cholesterolemia was established; and the platelet aggregation function, intracellular ionized calcium i, intracellular ionized magnesium i, cAMP, cGMP and inositol trisphosphate (IP 3) in platelet were examined with Flow cytometer, radioimmunoassay, inositol incoporation and so on. Results The occlusive thrombus formation time was lengthened and the platelet aggregation was inhibited significantly in API0134 group compared with model group. Meanwhile, the increase of platelet concentration of i, i, IP 3 in platelet induced by the thrombus formation were inhibited, and the cAMP concentration in platelet was increased markedly in API0134 treated group compared with control group. Conclusions API0134 exerts strong anti-thrombus and anti-platelet aggregation effects. The mechanism of anti-platelet aggregation is closely related to regulating the balance of intracellular i, i, cAMP and IP 3 in platelet.
关 键 词:API0134 高脂血症 家兔 血栓形成 血小板信号转导物质 中药 血小板聚集 钙转运ATP酶 三磷酸肌醇 实验研究
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.60