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人参强心滴丸治疗大鼠心力衰竭的作用机制研究 被引量:2

Mechanism of ren shen qiang xin di wan for rats with congestive heart failure
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摘要 目的研究人参强心滴丸治疗大鼠充血性心力衰竭(CHF)的作用机制。方法采用腹主动脉缩窄法复制CHF大鼠模型,分假手术组,模型组,人参强心滴丸高剂量组、低剂量组和对照组。采用流式细胞技术观察人参强心滴丸对CHF大鼠心肌细胞凋亡及相关调控基因bax和bcl-2蛋白表达的影响。结果模型组大鼠心肌细胞凋亡率明显升高,bax蛋白表达增强,bcl-2蛋白表达减弱;各用药组心肌细胞凋亡率明显下降,bax蛋白表达减弱,bcl-2蛋白表达增强。结论人参强心滴丸可调整bax和bcl-2的蛋白表达强度,降低心肌细胞凋亡率,逆转心室重塑,改善CHF预后。 [Objective] To investigate the effect of ren shen qiang xin di wan on cardiac muscle cell apoptosis and the related controlling genes of rats with congestive heart failure (CHF), and elucidate the therapeutic mechanism of ten shen qiang xin di wan on CHF. [Methods] The animal model of CHF was made by the method of abdominal aorta coarctation. Rats were randomly divided into sham group, CHF group, high doses of ten shen qiang xin di wan group, low dose of ten shen qiang xin di wan group, and positive control group (xin bao wan). Rat cardiac muscle cell apoptosis and the expression of apoptosis-related protein Bax and Bcl-2 were observed by flow cytometry. [Results] The rate of cardiocyte apoptosis was significantly increased in the rats with CHF. The expression of Bax was increased while the Bcl-2 expression was decreased in the cardiocytes from rats with CHF. Whereas in the three therapeutic groups with ten shen qiang xin di wan or xin bao wan, cardiocytes apoptosis rats were decreased significantly. Bax expression was decreased and Bcl-2 expression was increased. [Conclusion] Ren shen qiang xin di wan can reverse cardiac ventricle remodeling and improve the prognosis of heart failure by regulating the expression of Bax and Bcl-2, and reducing the rate of cardiocyte apoptosis.
出处 《山东医药》 CAS 北大核心 2006年第25期13-15,共3页 Shandong Medical Journal
基金 河北省科技厅研究与发展计划项目(04276101D-73)
关键词 人参强心滴丸 充血性心力衰竭 慢性 心肌细胞凋亡 BAX BCL-2 ren shen qiang xin di wan congestive heart failure, chronic cardiac muscle cell apoptosis bax bcl-2
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参考文献4

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