Objective To investigate the effect of licoflavone on aspirin-induced human gastric mucosal epithelial （GES-1） cell injury and its mechanism.Methods The study was conducted from March to November 2017.GES-1 cells were divided into 6 groups，control group （incubated with DMEM），aspirin group （incubated with 18.5 mmol/L aspirin for 24 h），low-dose，medium-dose and high-dose licoflavone groups （incubated with 18.5 mmol/L aspirin for 24 h after being pre-treated with 3，6，12 mg/L licoflavone for 2 h，respectively），PD98059 group （incubated with 18.5 mmol/L aspirin for 24 h after being pre-treated with 12 mg/L licoflavone for 2 h and with 10 μmol/L PD98059 for 1 h successively）．Proliferation inhibition rate was detected by MTT assay，apoptosis rate was measured by flow cytometry，lactate dehydrogenase （LDH），superoxide dismutase （SOD） activities，and malondialdehyde （MDA） content were determined by colorimetry，the protein expressions of p-ERK1/2，Bcl-2 and Bax were measured by western blotting.Results The control group showed significantly decreased proliferation inhibition rate，apoptosis rate，LDH activity，MDA content，and p-ERK1/2 and Bax expressions，but obviously increased SOD activity and Bcl-2 expression compared with other groups，as did the medium-dose and high-dose licoflavone groups and PD98059 group when compared with the aspirin group，and the PD98059 group when compared with the 3 licoflavone groups （P<0.05）．Conclusion Licoflavone alleviates aspirin-induced GES-1 cell injury through pro-proliferation，anti-apoptosis and anti-oxidative stress via the inhibition of ERK1/2 signaling pathway.
