Abstract: OBJECTIVE To explore the mechanisms of emodin in improving the lipopolysaccharide-induced cardiomyocyte injury. METHODS Lipopolysaccharides (LPS) were used to induce the in vitro model of myocardial injury. The H9C2 cells were divided into the Control group, the LPS group (treated with 25 mg/L of LPS), the Emodin group (treated with 25 mg/L of LPS plus 15 μMol/L of Emodin), and the 3-MA group (treated with 25 mg/L of LPS plus 15 μMol/L of Emodin plus 0.5 mmol/L of 3-MA). The survival rates of the cells were analyzed; the levels of lactic dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) were measured. The levels of interleukin (IL)- 1β, IL-6 and tumor necrosis factor- α(TNF-α) were detected by enzyme-linked immunosorbent assay. The expression levels of phosphatidylinositol 3-kinase (PI3K), phosphorylation of phosphatidylinositol 3-kinase (p-PI3K), protein kinase B (AKT), phosphorylation of protein kinase B (AKT), mammalian target of rapamycin (mTOR), phosphorylation of mTOR (p-mTOR), microtubule-associated protein light chain 3B (LC3B), sequestosome 1 (P62) and Beclin1 were determined by means of Western blotting. RESULTS The survival rates of cells of the LPS group were lower than those of the Control group; the levels of LDH, MDA, GSSG, IL-1β, IL-6 and TNF-α of the LPS group were higher than those of the Control group; the levels of SOD, GSH and GSH/GSSG of the LPS group were lower than those of the Control group; the expression levels of p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR and P62 protein of the LPS group were higher than those of the Control group; the levels of LC3B and Beclin-1 of the LPS group were lower than those of the Control group (all P＜0.05). The survival rates of cells of the Emodin group were higher than those of the LPS group; the levels of LDH, MDA, GSSG, IL-1β, IL-6 and TNF-α of the Emodin group were lower than those of the LPS group; the levels of SOD, GSH and GSH/GSSG of the Emodin group were higher than those of the LPS group; the expression levels of p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR and P62 protein of the Emodin group were lower than those of the LPS group; the levels of LC3B and Beclin-1 of the Emodin group were higher than those of the LPS group (all P＜0.05). The above effects were reversed when the autophagy inhibitor 3-MA was added. CONCLUSIONS The action mechanisms of Emodin in improvement of lipopolysaccharide-induced cardiomyocyte injury may be association with the inhibition of PI3K-AKT-mTOR signaling pathway level to activate autophagy and the inhibition of excessive oxidative stress and release of inflammatory cytokines.