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作 者:方晴霞[1,2] 邹小舟 俞文英[3] 方杰[3] 莫丽 余陈欢[3] FANG Qingxia;ZOU Xiaozhou;YU Wenying;FANG Jie;MO Li;YU Chenhuan(Department of Pharmacy,Zhejiang Provincial People's Hospital,Hangzhou 310053,Zhejiang,China;People's Hospital of Hangzhou Medical College,Hangzhou 310014,Zhejiang,China;Zhejiang Key Laborato- ry of Experimental Animal and Safety Evaluation,Zhejiang Academy of Medical Sciences,Hangzhou 310013,Zhefiang,China)
机构地区:[1]浙江省人民医院药学部 [2]杭州医学院附属人民医院 [3]浙江省医学科学院浙江省实验动物与安全性研究重点实验室
出 处:《中国临床药理学与治疗学》2018年第6期640-645,共6页Chinese Journal of Clinical Pharmacology and Therapeutics
摘 要: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.
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