水杨梅根黄酮类成分抑制血小板聚集和血栓形成的作用及机制研究

Inhibitory effect and mechanism of Adina rubella flavonoids on platelet aggregation and thrombosis

目的:研究水杨梅根黄酮类(adina rubella flavonoids,ARF)成分对血小板活化聚集及血栓形成的影响并对其机制进行初步研究。方法:利用不同的聚合剂5'-二磷酸腺苷(adenosine 5'-diphosphate,ADP)、花生四烯酸(arachidonic acid,AA)、血小板活化因子(platelet activating factor,PAF)诱导体外血小板聚集;分别建立ADP诱导的大鼠急性肺栓塞模型、小鼠尾部出血模型、大鼠动静脉旁路血栓模型,检测ARF对血小板聚集及血栓形成的抑制作用。Western blot检测CD41的蛋白表达及PI3K/Akt信号通路的活化情况。结果:ARF低、中、高剂量组能够显著提高急性肺栓塞大鼠存活率、延长小鼠尾部凝血时间、抑制动静脉旁路血栓模型大鼠血栓形成。ARF还能显著抑制ADP所诱导的血小板聚集及血小板标记蛋白CD41的上调及PI3K/Akt信号通路的活化。结论:ARF能够显著抑制血小板聚集及血栓形成,其机制可能与CD41/PI3K/Akt信号通路调控相关。

AIM： To investigate the effect and mechanism of Adina rubella flavonoids（ ARF） on platelet aggregation and activation. METHODS：Different stimulus [ adenosine 5 ＇-diphosphate（ ADP）,arachidonic acid（ AA）,platelet activating factor（ PAF） ]were used to induce platelet aggregation in vitro. A rat model of acute pulmonary embolism caused by ADP,a mouse model of bleeding time and a rat model of arteriovenous shunt thrombosis were established to observe the inhibitory effect of ARF on platelet aggregation and thrombosis. The expression of CD41 and the activation of PI3 K/Akt signal pathway were illustrated by Western blot.RESULTS： Compared with the control group,all ARF groups of the low-dose,middle-dose and highdose significantly improved the survival rates of acute pulmonary embolism rats,prolonged the bleeding time and inhibited arteriovenous shunt thrombosis formation. ARF also inhibited platelet aggregation,and up-regulated expression of CD41 and the activation of PI3 K/Akt signal pathway induced by ADP. CONCLUSION： ARF significantly inhibits the platelet aggregation and thrombosis,the mechanism may be related to CD41/PI3 K/Akt signaling pathway.