Objective To construct a mouse model of alcoholic liver fibrosis and explore the effect of supplementing exogenous thyroid hormone T3 on oxidative stress in liver. Methods  Eighty mice were randomly divided into 6 groups, normal control group, alcoholic liver fibrosis(ALF) model group, and low concentration T3 intervention group (25 μg/kg), medium concentration T3 intervention group (50 μg/kg), high concentration T3 intervention group (100 μg/kg) and T3 control group (the concentration of T3 is 100 μg/kg). A model of mice alcoholic liver fibrosis was established by using alcoholic liquid feed combined with 31.5% ethanol gavage. From the sixth week, mice in the T3 intervention and T3 control group were injected with corresponding concentrations of T3 intraperitoneally for three weeks. Mice in the control and T3 control groups were fed with control liquid feed. The degree of mice liver injury and fibrosis was evaluated through the sirius red staining, Western blotting, and serum biochemical testing. The activity of superoxide dismutase(SOD), the content of glutathione(GSH) and malondialdehyde(MDA) in liver tissue were detected by ELISA, and the protein expressions of microtubule-associated protein light chain 3-Ⅱ(LC3-Ⅱ) and p62 were detected by immunohistochemistry and Western blotting. Results  The liver structure and function in the ALF group were severely damaged, autophagy was inhibited, and the oxidative stress response was significantly enhanced compared with the control group. Compared with the ALF group, the recovery of liver functional and structure and autophagy were showed in the T3 intervention group, and SOD activity and GSH content in the liver increased in the low and medium concentrations of T3 intervention groups, while MDA content significantly decreased. In the high concentration T3 intervention group, it showed the same increase in SOD activity, a significant decrease in MDA content, while the content of GSH was lower than that in the control group, which was not different with the ALF group. Conclusion  Appropriate supplementation of T3 could affect the occurrence and development of alcoholic liver fibrosis by restoring the liver autophagy to inhibit the oxidative stress response.