Abstract: Objective   To investigate the effects of emodin on the energy metabolism of cardiomyocytes in rats with heart failure after myocardial infarction and its regulation mechanism on extra-cellular signal regulated kinase (ERK) signaling pathway.    Methods    The left anterior descending branch was ligated to construct a rat model of myocardial infarction. Successfully modeled animals were randomly divided into a model group, a low-dose group, a middle-dose group, a high-dose group and a control group according to the random number table method, each with 10 animals; at the same time, another 10 rats were taken as a sham operation group. Animals in the sham operation group were only threaded, but not ligated; rats in the low-dose group, middle-dose group, and high-dose group were treated with 20 mg/kg, 40 mg/kg, 60 mg/kg emodin by gavage every day. The rats in the control group were treated with captopril at 10 mg/kg. After 14 days of continuous administration, the left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), and ventricular septal thickness(IVS) of each group of rats were statistically analyzed. TUNEL staining was used to detect the apoptosis rate of rat cardiomyocytes. JC-1 staining was used to detect the mitochondrial membrane potential of rat cardiomyocytes. Western blot was used to detect the expressions of mitochondrial respiratory chain complex Ⅰ(complex Ⅰ) protein and p-ERK in myocardial tissue.    Results    Compared with the sham operation group, the LVEDD, LVESD, myocardial cell apoptosis rate, and the expression of complex I and p-ERK in myocardial tissue were significantly increased in the model group, low, medium, high dose group and the control group. LVEF, IVS and the mitochondrial membrane potential of cardiomyocytes were significantly reduced, and the differences were statistically significant (all P<0.05). Compared with  the modern group, the LVEDD, LVESD, myocardial cell apoptosis rate, and the expression of complex I and p-ERK in myocardial tissue were significantly reduced in the low, medium, high dose group and the control group. LVEF, IVS and the mitochondrial membrane potential of cardiomyocytes were increased significantly, and the differences were statistically significant (all P<0.05).    Conclusions    Emodin can significantly improve the mitochondrial damage and energy metabolism in heart failure rats after myocardial infarction, reduce the apoptosis rate of myocardial tissue, and improve the cardiac function of experimental animals.

Key words: Emodin, Myocardial infarction, Heart failure, Energy metabolism, Extra-cellular signal regulated kinase signaling pathway