摘要
目的探讨生脉注射液对阿霉素心肌损伤的作用是否为通过抗细胞凋亡机制。方法腹腔注射阿霉素建立大鼠阿霉素心肌损伤模型。观察大鼠心率变化,计算死亡率;测定各组大鼠肌酸激酶同工酶(CK-MB);TUNEL法检测细胞凋亡;免疫组化检测Bax、Bcl-2蛋白水平表达;RT-PCR检测Bax、Bcl-2mRNA水平表达。结果生脉注射液在蛋白、mRNA水平可明显使Bcl-2表达增加,Bax表达减少;减少CK-MB释放,减少死亡率。与模型组比较均有显著性意义(P<0.01或0.05),其疗效成一定剂量依赖性。结论生脉注射液对大鼠阿霉素心肌损伤有明显疗效,其机制可能与抑制细胞凋亡等作用有关。
Objective To investigate whether the mechanism of Shengmai injection on adriamycin-induced myocardium injury in rats is inhibiting the apoptosis. Methods The rat model of myocardium injury was made by injecting adriamycin into the pleural. The changes of heart rate were detected. The death rate was calculated. Cell apoptosis was detected by TUNEL. The measurements of CK-MB were detected. The expression level of Bax, Bcl-2 pertain and mRNA were detected by immunhistochemical method and RT-PCR. Results Shengmai Injection significantly increased the expression level of Bcl-2 protein and mRNA, while significantly reduced Pax protein. It reduced the serum CK-MB concentration, reduced the apoptosis index and the death rate （P〈0.01 or 0.05）, but it was somewhat close-dependent. Conclusion Shengmai injection can obviously decrease the adriamycin-induced myocardium injury in rats and protect myocardium, whose mechanism may be inhibiting the apoptosis.
出处
《中南药学》
CAS
2008年第2期162-165,共4页
Central South Pharmacy
关键词
生脉注射液
心肌损伤
自由基
细胞凋亡
阿霉素
shengmai injection
myocardium injury
oxygen radical
apoptosis
adriamycin
