Liang Tuo, Zhang Yuhui, Yin Shijie, Gan Tianyi, An Tao, Zhang Rongcheng, Wang Yunhong, Huang Yan, Zhou Qiong, Zhang Jian
State Key Laboratory of Cardiovascular Disease, Heart Failure Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 10037, China.
Am J Transl Res. 2016 May 15;8(5):2047-58. eCollection 2016.
Qiliqiangxin (QL) capsule is a traditional Chinese medicine which has been approved for the treatment of chronic heart failure. Evidences proved that QL capsules further reduced the NT-proBNP levels and improved left ventricular ejection fraction in CHF patients but the evidence supporting its underlying mechanism is still unclear.
Myocardial infarction (MI) -Heart failure (HF) Sprague-Dawley ratsmodel and neonatal rat cardiac myocytes (NRCMs) were used. Animals were assigned into 4 groups, normal group (n=6), shame-operation group (n=6), MI rats 4 weeks after left anterior descending coronary artery ligation were randomized into vehicle group (n=8), QL group (n=8). QL significantly attenuated cardiac dysfunction and ventricle remodeling as echocardiography and hemodynamic measurements showed improvement in left ventricular ejection fraction, fractional shortening, ±dp/dt and left ventricular end diastolic and systolic diameters in QL treated group compared with the vehicle group. Improvements ininterstitial fibrosisand mitochondrial structures were also exhibited by Sirius Red staining, RT-PCR and electron microscopy. QL treatment improved apoptosis and VEGF expression in rats marginal infract area. Complementary experiments analyzed the improved apoptosis and up-regulate of VEGF in ischemia-hypoxia cultivated NRCMs is in an Akt dependent manner and can be reversed by Akt inhibitor.
QL capsule can improve cardiac dysfunction and ventricular remodeling in MI-HF ratsmodel, this cardiac protective efficacy may be concerned with attenuated apoptosis and cardiac fibrosis. Up-regulated VEGF expression and Akt phosphorylation may take part in this availability.
芪苈强心胶囊是一种已被批准用于治疗慢性心力衰竭的中药。有证据表明,芪苈强心胶囊可进一步降低慢性心力衰竭患者的N末端B型利钠肽原(NT-proBNP)水平并提高左心室射血分数,但支持其潜在机制的证据仍不明确。
采用心肌梗死(MI)-心力衰竭(HF)的Sprague-Dawley大鼠模型和新生大鼠心肌细胞(NRCMs)。将动物分为4组,正常组(n = 6)、假手术组(n = 6),左冠状动脉前降支结扎4周后的MI大鼠随机分为溶剂对照组(n = 8)、芪苈强心组(n = 8)。超声心动图和血流动力学测量结果显示,与溶剂对照组相比,芪苈强心组左心室射血分数、缩短分数、±dp/dt以及左心室舒张末期和收缩末期直径均有改善,表明芪苈强心能显著减轻心脏功能障碍和心室重构。天狼星红染色、逆转录-聚合酶链反应(RT-PCR)和电子显微镜检查也显示间质纤维化和线粒体结构有所改善。芪苈强心治疗改善了大鼠梗死边缘区的细胞凋亡和血管内皮生长因子(VEGF)表达。补充实验分析了缺血缺氧培养的NRCMs中细胞凋亡的改善和VEGF的上调是以蛋白激酶B(Akt)依赖的方式进行的,并且可被Akt抑制剂逆转。
芪苈强心胶囊可改善MI-HF大鼠模型的心脏功能障碍和心室重构,这种心脏保护作用可能与减轻细胞凋亡和心脏纤维化有关。VEGF表达上调和Akt磷酸化可能参与了这一作用机制。