摘要
目的:探讨复元胶囊诱导气虚血瘀证大鼠血管平滑肌细胞(VSMCs)凋亡的作用及其分子机制。方法:采用缺口末端标记(Terminal deoxynucleotidy1 transferase mediated dUTP nicked labeling,TUNEL)法检测VSMCs凋亡,计算VSMCs凋亡指数(SMAI)、透射电镜检测细胞形态学变化;应用免疫组织化学法检测bcl-2和bax蛋白表达。结果:与正常对照组比较,模型组VSMCs中的bcl-2蛋白表达明显增强(P<0.05),SMAI明显减少(P<0.01),bax蛋白表达无显著改变(P>0.05);与模型组组比较,复元胶囊组VSMCs的bcl-2蛋白表达显著减少(P<0.05),bcl-2/bax比值下降,SMAI增加(P<0.05)。结论:复元胶囊促进了气虚血瘀证大鼠的VSMCs凋亡,可能机制是通过调节VSMCs的bcl-2/bax蛋白表达平衡。
Objective： To determine the effect of the recipe Fuyuan capsule on apoptosis and its mecha- nisms in vascular smooth muscle cells （VSMC） from rats with Qi deficiency and blood stasis. Methods： The expressions of bcl-2 and bax proteins were determined by immunohistochemical staining. Apoptosis of VSMCs was identified by in situ TdT-mediated dUTP nick end labeling （TUNEL）, and smooth muscle cell apoptotic index （SMAI） was determined by semi-quantitative analysis. Results： Compared with normal control, the expression of bcl-2 protein was increased （P 〈0.05）, SMAI was decreased （P 〈0.01 ）, but the bax expression did not significantly change in rats with Qi deficiency and blood stasis. After treatment with Fuyuan, the increased expression of bcl-2 protein was decreased （P 〈 0.05） , the ratio of bcl-2/bax were significantly lower, and SMAI was increased significantly （P 〈 0.05）. Conclusion ： Fuyuan capsule promotes the apoptosis of VSMC in rats with Qi deficiency and blood stasis, which may relate to the expression balance of bcl-2/bax in VSMCs.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2009年第9期839-843,共5页
Chinese Journal of New Drugs
基金
重庆市卫生局科研项目(C03050401)
关键词
复元胶囊
气虚血瘀
血管平滑肌细胞
凋亡
Fuyuan capsule
Qi deficiency and blood stasis
vascular smooth muscle cells
apoptosis
