Abstract: Objective To investigate the mechanism of Elabela in myocardial ischemia / reperfusion injury. Methods The concentrations of Elabela in patients with acute ST-segment elevation myocardial infarction （STEMI） were detected. The expression and function of Elabela in H9C2 cells （rat embryonic heart clone cell line） were evaluated by obtaining clinical blood samples and establishing an oxidative stress model in vitro to simulate ischemia / reperfusion injury. Results The concentration of Elabela in the plasma of STEMI patients and the expression of Elabela in H9C2 cells treated with H₂O₂ were both up-regulated （both P < 0.001）. Elabela could reduce the level of Bax, the rates of cardiomyocyte apoptosis, the number of reactive oxygen species-positive cells, the levels of lactate dehydrogenase and malondialdehyde, whereas increased superoxide dismutase activity and Bcl-2 expression in H₂O₂ treated H9C2 cells （all P < 0.05）. The inhibition of α7nAChR/JAK2/STAT3 signaling pathway by the specific inhibitor α-ring snake toxin partially counteracted the protective effect of Elablela. Conclusion Elabela ameliorates H₂O₂-induced H9C2 cell injury by activating the α7nAChR/JAK2/STAT3 signaling pathway.