Background: The paper aimed to investigate the effects of Maslinic acid on myocardial injury caused by ischemia and hypoxia after acute myocardial infarction, and to explore the mechanism of Maslinic acid inhibiting local inflammation and myocardial cell pyrolysis, slowing down the synthesis of extracellular matrix, improving myocardial fibrosis and remodeling ventricle. Materials and Methods: Wistar rats with acute myocardial infarction were used. The serum levels of TNF-α, IL-1β, CRP, and LDH were detected by ELISA. The expressions of inflammation-related proteins such as TLR4, NFκB, NLRP3, IL-10, and TGF-β in myocardial infarction were detected by Western-blot. TUNEL method was employed to detect myocardial cell pyrolysis. Masson staining was used to detect myocardial fibrosis. Immunohistochemical method was applied to detect the expressions of CD206 and CD11C to understand the polarization of macrophages. Results: Maslinic acid can inhibit the levels of inflammatory factors such as CRP, TNF-α and IL-1β, and reduce the expression of myocardial TLR4, NFκB, NLRP3 and other inflammation-related proteins after myocardial infarction. The release of LDH is significantly reduced. The expression of TUNEL positive cells in myocardium is obviously reduced after myocardial infarction. Maslinic acid can increase the expression of CD206-positive cells and reduce the expression of CD11C-positive cells, thus regulate and promote polarization into M2 macrophages. Conclusion: Maslinic acid may inhibit myocardial cell pyrolysis and inflammatory response by regulating the TLR4/NFκB/NLRP3 signaling pathway. Maslinic acid can improve myocardial fibrosis by inhibiting myocardial cell pyrolysis and regulating the polarization of macrophages.