Objective: Explore the effect and mechanism of Liguzinediol on cardiac function in myocardial infarction rats. Methods: The model of heart failure after myocardial infarction was established by ligating the left anterior descending coronary artery of rats. Different doses of Liguzinediol (5,10,20mg/kg) and digoxin (0.0332mg/kg) were used for the treatment of the rats for 12 weeks. Cardiac function was detected by echocardiography. serum myocardial injury marker brain natriuretic peptides (BNP), lactate dehydrogenase (LDH) and myocardial tissue adenosine triphosphate (ATP) content were detected by the detection kit; HE staining was used for observing myocardial morphology; electron microscopy was used to detect mitochondrial morphology; the expressions of mitochondrial dynamics and autophagy related proteins were detected by Western blot (WB); and immunohistochemical staining was used to detect the expression of mitophagy related proteins. The cardiomyocyte model was replicated by oxygen and glucose deprivation (OGD). The expression of mitophagy-related proteins was detected by WB, and mitophagy levels were detected by LC3B adenovirus transfection Mitochondrial membrane potential, reactive oxygen species (ROS) level and apoptosis were detected by fluorescence labeling. Results: Liguzinediol significantly increased ejection fraction (EF), Fractional shortening (FS), and decreased left ventricular dimension in systole (LVIDs) in myocardial infarction rats. Liguzinediol significantly reduced serum BNP and LDH in myocardial infarction model rats, and increase the level of ATP in the heart of myocardial infarction rats. Liguzinediol improved the morphology of cardiomyocytes and mitochondria in the hearts of myocardial infarction rats, and regulated the expression of mitochondrial dynamics-related proteins and promoted autophagy in the hearts of myocardial infarction rats. In vitro, Liguzinediol reduced ROS content in OGD model of H9C2 cells, promoted mitophagy and fusion, protected mitochondrial membrane potential, and reduced H9C2 cell apoptosis. The combined use of autophagy agonist and Liguzinediol partially increased the protective effect of Liguzinediol on OGD model of H9C2 cells, while autophagy inhibitor completely abolished the regulatory effect of Liguzinediol on mitochondria of GD model of H9C2 cells and canceled its inhibitory effect on apoptosis of GD model of H9C2 cells. Conclusion: Liguzinediol can promote mitochondrial autophagy and fusion, maintain mitochondrial morphology and function integrity, reduce cardiomyocyte apoptosis, and improve cardiac function myocardial infarction rats.