Objective: To investigate the effect of Qiangxin Huoli decoction on rats with chronic heart failure (CHF) induced by adriamycin (ADR), and to investigate the underlying mechanism of this effect.
Methods: Ninety-six healthy Wistar rats were divided into six groups: control, CHF model, CHF treated by Shenfu injection, and three CHF groups treated with Qiangxin Huoli decoction at high, medium, and low doses, respectively. Qiangxin Huoli decoction was administered orally to protect the stomach in the three Qiangxin Huoli decoction groups, while the control group and the CHF model group were administered the same volume of 0.9% physiological saline, and the Shenfu group wereadministered the same volume of Shenfu injection. Ten days later, the CHF model was then induced in all groups except the control group by intraperitoneal injection of ADR at gradient dose intervals. The bodyweights were recorded on days 10, 20, 30, and 40. Hemodynamic indices were recorded, including left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximum increase in left ventricular pressure (+dp/dtmax), maximum decrease in left ventricular pressure (-dp/dtmax), heart rate (HR), and electrocardiogram using an eight-channel physiological recorder with LabChart software monitoring. The plasma brain natriuretic peptide (BNP) concentration was determined by enzyme-linked immunosorbent adsorption. The expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected by immunohistochemical methods.
Results: The CHF model group were in poor condition, and the mean bodyweight was significantly decreased compared with the control group. Furthermore, compared with the control group, the CHF groups had significantly decreased LVSP, +dp/dtmax, and -dp/dtmax, and significantly increased LVEDP. The CHF groups also showed significant increases in HR, S-T segment elevation, and plasma BNP levels compared with the control group. Compared with the CHF model group, the treatment groups had significantly increased Bax expression (P < 0.05) and significantly decreased Bcl-2 expression (P < 0.01), indicating less apoptosis. The high dose Qiangxin Huoli decoction group and the Shenfu group showed the most significant improvements.
Conclusion: In the rat model of CHF, Qiangxin Huoli decoction significantly reduces the abnormal hemodynamics, improves cardiac function, reduces plasma BNP concentration, regulates the expression of apoptosis proteins, inhibits the apoptosis of myocardial cells, and plays a protective role.
Keywords: Bcl-2-associated X protein; Doxorubicin; Genes, bcl-2; Heart failure; Hemodynamics; Natriuretic peptide, brain; Qiangxin Huoli decoction.