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Intervention of multiple pathways by multiple active components provides potent protection against cerebral ischemia injury

多成分、多途径同时干预提供强效抗脑缺血作用(英文)

作     者:张精亮 胡涛 刘晓岩 朱元军 王银叶 Jingliang Zhang;Tao Hu;Xiaoyan Liu;Yuanjun Zhu;Yinye Wang

作者机构:北京大学医学部药学院分子与细胞药理学系北京100191 

出 版 物:《Journal of Chinese Pharmaceutical Sciences》 (中国药学(英文版))

年 卷 期:2014年第23卷第5期

页      面:295-301页

核心收录:

学科分类:1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基  金:National Natural Science Foundation of China(Grant No.81302763) Beijing Natural Science Foundation(Grant No.7144218) 

主  题:Multiple pathways Multiple components Cerebral ischemia/reperfusion injury Formula 2 

摘      要:To explore the effect of multiple pathway intervention in acute cerebral ischemia injury, we prepared a medicine formula (formula 2) consisting of ginsenosides, pueraria flavonoids, ophiopogonis and borneol as a tool medicine. The effects of formula 2 and its components on PC12 cell viability and potential pathway were investigated, and the influence of this formula on venous thrombosis and platelet aggregation was also assessed, then the effect of formula 2 on middle cerebral artery occlusion (MCAO) reperfusion was observed in rats. Formula 2 markedly enhanced the cell viability, which was stronger than that of each individual component. Formula 2 significantly inhibited the NO production in PC12 cells induced by H202, and this effect was also stronger than that of each individual component. Moreover, formula 2 enhanced the SOD activity, and the effect was stronger than that of ginsenosides. In addition, formula 2 reduced the MDA content, and this effect was stronger than that of ophiopogonins. In vivo, formula 2 showed potent inhibitory effects on platelet aggregation and venous thrombosis. Furthermore, formula 2 (single dose, s.c.) significantly reduced the infarct volume and neurobehavioral scores in MCAO reperfusion rats. Take together, our results suggests that formula 2 has powerful ability of inhibiting the ischemia/reperfusion injury, and this effect might be attributed to its simultaneous intervention in the cascade reaction of neuronal injury via multiple pathways contributed by multiple components during cerebral ischemia/reperfusion.

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