黄芪、当归对血管内皮剥脱后内膜增生的影响及作用机制  

Effect of astragalus membranaceus and angelica sinensis on vessel restenosis

作　　者：李琦[1] 温进坤[1] 韩梅[1] 

机构地区：[1]河北医科大学基础医学研究所生化室,河北石家庄050017

出　　处：《中国老年学杂志》2003年第11期758-760,共3页Chinese Journal of Gerontology

基　　金：国家自然科学基金 (39970 2 74);河北省自然科学基金(30 1 358)资助

摘　　要：目的　研究黄芪和当归防治血管内皮剥脱后再狭窄与血管平滑肌细胞 (VSMC)表型转化之间的关系。方法　建立大鼠主动脉内皮剥脱模型 ,分别采用形态学和 Northern印迹分析技术 ,观察大鼠血管内皮剥脱后内膜增生情况及 VSMC表型标志基因 SMα-肌动蛋白、平滑肌胚胎型肌球蛋白重链 (SMemb)表达活性。结果　术后 7d模型组内膜明显增生 ,1 4～ 2 1 d内膜呈进行性弥漫性增厚。与模型组相比 ,两种中药治疗组的内膜增生程度均明显减轻 ;分化标志 SMα-肌动蛋白基因表达增高 ,去分化标志 SMemb表达降低。结论　黄芪和当归通过抑制 VSMC表型转化而减缓血管内膜增生。Objective To explore the relationship between effect of Astragalus membranaceus (Ast) and Angelica sinensis (Ang) on vessel restenosis and phenotypic remodeling of vascular smooth muscle cells (VSMC).Methods The vessel restenosis model was established by denuding the rat arterial endothelium with balloon catheter. Northern blot and pathological analysis were used, respectively, to detect the effects of Ast and Ang on VSMC phenotypic marker genes SM α-actin and SMemb and the intima hyperplasia.Results Seven days after de-endothelialization, the intima thickening was observed obviously. On the 14~21th, the hyperplasia was progressive and diffuse.In the group treated by Ast and Ang , the hyperplasia was showed but notably weaker than that of the model after vascular injury.The expression activity of differentiated marker gene SM α-actin was higher,however,the dedifferentiated marker SMemb was lower in the Ast and Ang group than that of the model group. Conclusions Ast and Ang could reduce intima hyperplasia by inhibiting VSMC phenotypic remodeling.

关 键 词：黄芪 当归 内膜增生 作用机制 血管平滑肌细胞 血管再狭窄 药理作用 

分 类 号：R259.43[医药卫生—中西医结合] R285.5[医药卫生—中医内科学]