ObjectiveTo explore the possible mechanism of Dipteris sinensis (Kudiezi) on cardiac function in rats with heart failure (HF).MethodsThirty rats were randomly divided into three groups: control group, HF group and HF+Kudiezi group (n=10 in each group). Echocardiography was performed to determine cardiac function, including LVEF, LVFS, LVEDD, LVESD. HE staining was used to examine myocardial pathological changes. Cardiomyocyte cross-sectional area was measured by WGA staining, and myocardial cell apoptosis was assessed by TUNEL kit. Mitochondrial ultra-structure was examined by transmission electron microscope. Western blotting was used to assess the protein levels of Bcl-2, Bax, Cyto c and Caspase-1 in myocardial tissues.ResultsCompared with the control group, LVEF and LVFS were decreased, LVEDD and LVESD were increased in the HF group (P<0.05). Myocardial tissue structure was shown to be loose and disordered, with increased cross-sectional areas and apoptosis of myocardial cells (P<0.05). The mitochondria became swelling, associated with abnormal morphology and reduced number of mitochondrial cristoid in myocardial tissues. Similarly, the expression of Bcl-2 protein in myocardial tissues was decreased, and the expression of mitochondrial apoptosis pathway proteins Bax, Cyto c and Caspase-1 protein was elevated (all P<0.05). Compared with the HF group, both LVEF and LVFS were increased, LVEDD and LVESD were decreased, myocardial structural distortion, myocardial cell cross-sectional area, and apoptosis were decreased, and myocardial mitochondrial structure was improved in the HF+Kudiezi group (all P<0.05). The expression levels of Bcl-2 protein in myocardial tissues were increased, and those of Bax, Cyto c and Caspase-1 proteins were reduced (P<0.05).ConclusionDipteris sinensis (Kudiezi) can improve cardiac function in HF rats by down-regulating mitochondrial apoptosis.