白术内酯Ⅱ抗血小板作用及对血小板中蛋白激酶B磷酸化水平的影响  

Influence of atractylenolide Ⅱ on platelet and phosphorylation level of protein kinase B

作　　者：陈一竹 杨文龙[1] 郭玲玉[1] 张明亮[1] 刘俊岭[2] 张俊峰[1] 

机构地区：[1]上海交通大学医学院附属第九人民医院心内科,上海201900 [2]上海交通大学医学院基础医学院,上海200025

出　　处：《中国医药导报》2016年第11期18-21,26,共5页China Medical Herald

基　　金：上海交通大学医学院附属第三人民医院自然科学研究基金资助项目(syz2015-002)

摘　　要：目的观察白术内酯Ⅱ在体外对小鼠和人血小板活化的影响,并探讨其可能的分子机制。方法通过体外血小板聚集实验,采用比浊法测定不同浓度白术内酯Ⅱ对胶原诱发的小鼠及人血小板聚集的影响;通过血小板的铺展实验,检测白术内酯Ⅱ对人血小板铺展的作用;运用Western blot检测人血小板中蛋白激酶B(Akt473)的磷酸化水平。结果白术内酯Ⅱ可抑制胶原刺激下小鼠和人血小板的体外聚集(P<0.01);经白术内酯Ⅱ处理后的人血小板铺展面积缩小(P<0.01);人血小板中Akt473分子的磷酸化水平降低(P<0.01)。结论白术内酯Ⅱ对胶原诱导的小鼠和人血小板聚集能产生显著抑制作用,对人血小板的铺展也有抑制作用,其作用机制可能与血小板活化过程中的PI3K-Akt信号通路有关,提示白术内酯Ⅱ是一种有效的抗血小板化合物。Objective To observe the effects of the atractylenolide Ⅱ on mice and human platelet in vitro and discuss the underlying mechanism. Methods The effect of atractylenolide Ⅱ on mice and human platelet aggregation was induced by collagen in vitro. The effect of atractylenolide Ⅱ on human platelet was detected through the experiment of spreading. The phosphorylation level of Akt473 was detected by Western blot. Results Atractylenolide Ⅱ inhibited collagen-induced mice and human platelet aggregation（P〈0.01）, and the spreading of human platelets on immobilized fibrinogen treaded with atractylenolide Ⅱ was diminished（P〈0.01）. The level of phospho-Akt 473 was downregulated in the presence of atractylenolide Ⅱ（P〈0.01）. Conclusion These results show that atractylenolide Ⅱ affected the platelet aggregation and spreading, and through regulating the PI3K-Akt signal way to inhibit platelet activities, atractylenolide Ⅱ is an effective antiplatelet compounds.

关 键 词：白术内酯Ⅱ 血小板 血栓 蛋白激酶B 

分 类 号：R285.5[医药卫生—中药学]