Background: The majority of myocardial infarction (MI) cases occur due to plaque rupture in the context of atherosclerosis (AS). This study aimed to elucidate the mechanisms underlying the effect of Methods: Apolipoprotein E-deficient mice were divided into four groups of 11. Mice in the Control and MI groups were fed a normal diet for 24-weeks, while mice in the AS + MI group were fed a high-fat diet (HFD) and mice in the AS + MI + HAL group were fed HFD supplemented with 5% HAL powder. After 23 weeks, the mice in the MI, AS + MI and AS + MI + HAL groups underwent coronary artery ligation to induce MI. A week post-ligation, 6 surviving mice were randomly selected from each group for the subsequent experiments, echocardiography was performed, followed by analysis of aortic plaque and myocardial tissue to explore potential mechanisms. Results: HAL intervention attenuated cardiac remodeling and dysfunction induced by MI, reduced inflammatory cell infiltration and fibrosis in the myocardium, and consequently improved cardiac function. HAL alleviated the inflammatory response by reducing serum concentrations and myocardial expression of interleukin-1β, interleukin-6 and tumor necrosis factor-α. Furthermore, Western blotting analysis demonstrated that HAL reduced nuclear factor-κB (NF-κB) expression. HAL also enhanced superoxide dismutase and glutathione peroxidase levels while suppressing malondialdehyde and myeloperoxidase levels in cardiac infarction tissue. Conclusion: Our data indicated that HAL attenuates cardiac remodeling by inhibiting inflammation and reducing oxidative stress. These findings provide novel insights into the effects and mechanisms of HAL in the context of MI.