Journal of Jilin University(Medicine Edition) ›› 2020, Vol. 46 ›› Issue (05): 972-978.doi: 10.13481/j.1671-587x.20200512

• Research in basic medicine • Previous Articles    

Inhibitory effect of Qisheng-Yiqi Dropping Pill on apoptosis of myocardial cells in rats with chronic heart failure and its mechanism

CHEN Jiaxian1, LIU Xianxia1, CHEN Yuewu1, CHEN Lei1, ZHANG Yuansheng1, CHEN Jinsong2   

  1. 1. Department of Cardiovascular Medicine, Second Affiliated Hospital, Hainan Medical University, Haikou 570311, China;
    2. Department of Cardiovascular Medicine, Second Affiliated Hospital, South China University, Hengyang 421001, China
  • Received:2020-01-11 Published:2020-10-23

Abstract: Objective: To investigate the effect of Qishen-Yiqi Dropping Pill (QSYQ) on the apoptosis of myocardial cells in the rats with chronic heart failure (CHF), and to explore its possible mechanism. Methods: Sixty male SD rats were randomly divided into sham operation group, model group, positive drug control group (6.75 mg·kg-1·d-1 Captopril), low dose (135 mg·kg-1·d-1) of QSYQ group and high dose (270 mg·kg-1·d-1) of QSYQ group, and there were 12 rats in each group. The CHF models were established by ligating anterior descending coronary artery. After successful establishment of the models,the rats were continuously administrated by gavage for 4 weeks; the cardiac function was measured by echocardiography and the apoptotic rate of myocardial cells was detected by TUNEL assay. The activities of serum lactate dehydrogenase (LDH) and superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) of the rats were determined by colorimetry, the reactive oxygen species (ROS) levels in myocardium tissue of the rats were detected by flow cytometry, and the expression levels of apoptosis-related proteins, Nrf2 and HO-1 proteins in myocardium tissue of the rats were detected by Western blotting method. Result: Compared with sham operation group, the left ventricular end-systolic diameter (LVSD) and left ventricular end-diastolic diameter (LVDD) of the rats in model group were significantly increased (P<0.05), and the left ventricular ejection fraction (EF), and left ventricular short-axis shortening rate (FS) were significantly decreased (P<0.05); the number of brown and yellow myocardial cells was increased(P<0.05), and the apoptotic rate was significantly increased (P<0.05);the LDH activity and the ROS and MDA levels in serum were significantly increased (P<0.05),and the SOD activity was significantly decreased (P<0.05); the expression levels of Cleaved-Caspase-3 and Bax protein in myocardium tissue were significantly increased (P<0.05), and the expression levels of Bcl-2, Nrf2 and HO-1 proteins were significantly decreased (P<0.05). Compared with model group, the LVSD and LVDD of the rats in high dose of QSYQ group and positive drug control group were significantly decreased (P<0.05), EF and FS were significantly increased (P<0.05); the number of brown and yellow myocardial cells was decreased (P<0.05), the apoptotic rates were significantly decreased (P<0.05), the LDH activities and the ROS and MDA levels in serum were significantly decreased (P<0.05), and the SOD activities were significantly increased (P<0.05); the expression levels of Cleaved-Caspase-3 and Bax proteins in myocardium tissue of the rats were significantly decreased (P<0.05), and the expression levels of Bcl-2 protein were significantly increased (P<0.05); there were no significant differences in the above indexes of the rats between low dose of QSYQ group and model group (P>0.05). Compared with model group, the expression levels of Nrf2 and HO-1 proteins in myocardium tissue of the rats in high dose of QSYQ group were significantly increased (P<0.05); there were no significant differences in the expression levels of Nrf2 and HO-1 proteins in myocardium tissue of the rats between low dose of QSYQ group and positive drug group (P>0.05). Conclusion: QSYQ can inhibit the apoptosis of myocardial cells in the rats with CHF, and its mechanism may be related to activating the Nrf2/HO-1 signaling pathway and reducing the oxidative damage.

Key words: chronic heart failure, Qishen-Yiqi Dropping Pill, myocardial cells, nuclear factor E2/Heme oxidase-1 signaling pathway

CLC Number: 

  • R541.6