Objective To investigate the protective effect of edaravone on sepsis-related myocardial injury in rats. Methods Seventy eight healthy male Sprauge-Dawley (SD) rats were randomly divided into normal group (Norm), sham operation group (Sham), sepsis group (CLP), low-dose edaravone treated group (ED1) and high-dose edaravone treated group (ED2). A rat model of sepsis-related myocardial injury was developed by cecal ligation and puncture (CLP). Edaravone was administered to the rats in ED1 and ED2 group. Serum cardiac troponin I (cTnI) was measured, and hydroxyl radicals (OH-), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were examined in the heart tissue at various time points (3 h, 6 h, and 12 h after operation). Myocardial pathomorphology was also observed. Results Changes of all indexes were not significantly different between Norm group and Sham group (P > 0.05). In ED1 and ED2 group, cTnI, OH-, MDA, TNF-α, and IL-1β were significantly higher than in Norm and Sham group, but lower than in CLP group; SOD was significantly lower than in Norm and Sham group, but higher than in CLP group (P < 0.01). In ED2 group, cTnI, OH-, MDA, TNF-α, and IL-1β were significantly lower, but SOD was significantly higher than in ED1 group (P < 0.01). Myocardial pathomorphology in CLP group included edema, congestion in mesenchyma, and inflammatory cells infiltration were not significantly changed in Norm group and Sham group, but alleviated evidently in ED1 group and ED2 group. Conclusions Edaravone alleviates sepsis-related myocardial injury, which probably related to the inhibition of oxidative stress and cytokines. High-dose edaravone (6 mg/kg) is more efficient than low-dose (3 mg/kg) in protective effect on sepsis-related myocardial injury.