Objectives: To study the protective effect of camel milk on alcoholic liver injury in mice induced by Lieber-DeCarli liquid diet. Methods: 40 male C57BL/6NCr mice were randomly divided into control group(Con)， model group (Et)， camel milk high-dose group (EtCM_H， 3 g/kg)， camel milk low-dose group (EtCM_L， 1.5 g/kg) and positive control group (Metadoxine， 300 mg/kg). The experiment was conducted for a total of 8 weeks. The first 4 weeks were only fed with special feed without gavage. After 4 weeks， the feeding method was unchanged， with milk or metadoxine by gavage， once a day. After intragastric administration， the NIAAA model was established by intragastric administration of 31.5% alcohol solution at a dose of 5 g/kg. The indicators of liver antioxidant and anti-inflammatory， apoptosis markers contents， serum transaminase activity were measured. HE staining was used to observe liver histopathological changes. Oil Red O staining was used to observe liver lipid accumulation. TUNEL staining was used to detect liver cell apoptosis. Results: Camel milk could significantly reduce the activities of serum alanine aminotransferase and aspartate aminotransferase in mice with liver injury， and reduce liver tissue malondialdehyde， triglycerides， and tumor necrosis factor-α (TNF-α)， interleukin-1β (IL-1β)， interleukin-6 (IL-6) content and Caspase-3 activity， improve the activity of superoxide dismutase in mouse liver tissue， reduce glutathione and interleukin-10 (IL-10) content， reduce lipid accumulation in the liver， reduce liver cell edema， and antagonize liver cell apoptosis. Conclusion: Camel milk has a protective effect on alcoholic liver injury induced by Lieber-DeCarli liquid diet in mice， and presents a dose-dependent characteristic. High dose is better than low dose. Camel milk may improve liver cell antioxidant capacity and increase the content of inflammatory factors to promote fat transport， and then restore the structure and function of liver cells to achieve this protective effect.