OBJECTIVETo investigate the effects of Xinfuli Granule (XG) on cardiomyocyte apoptosis in rats with adriamycin-induced dilated cardiomyopathy (DCM).

METHODSSeventy-two male SD rats were randomly divided into 6 groups, i.e., the normal control group, the model group, the irbesartan group, the low dose XG group, the medium dose XG group, and the high dose XG group. The DCM heart failure rat model was established using peritoneal injection of ADR. Equal volume of normal saline was injected to those in the normal control group, once per week for 6 consecutive weeks. The medication was started from the 5th week by gastrogavage. XG was dispensed into 0.5 g/mL suspension with distilled water. The XG was administered at the daily dose of 0.675 g/kg, 1.350 g/kg, and 2.700 g/kg to those in the low dose XG group, the medium dose XG group, and the high dose XG group, respectively. Irbesartan was administered to rats in the irbesartan group at the daily dose of 50 mg/kg. Equal volume of normal saline was administered to those in the normal control group and the model group by gastrogavage, once in the morning for 4 consecutive weeks. Myocardial apoptosis was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the expressions of the Bcl-2 and Bax protein of cardiomyocytes were measured by immunohistochemical assay.

RESULTSCompared with the normal control group, the cardiomyocyte apoptosis rate and Bax expression level obviously increased, but the expression of Bcl-2 and the Bcl-2/Bax ratio decreased significantly in the model group (P < 0.05). Compared with the model group, the expression of Bax and the Bcl-2/Bax ratio increased significantly in the high dose XG group and the irbesartan group (P < 0.01). The Bax expression level obviously decreased in all groups except the normal control group (P < 0.01).

CONCLUSIONSXG could obviously attenuate cardiomyocyte apoptosis in the adriamycin-induced DCM rats, and reverse the occurrence and development of heart reconstruction. The underlying mechanism might be related to regulating and controlling the expressions of Bax and Bcl-2.