Objective: To explore the molecular mechanism of camel milk to relieve acute alcoholic liver injury in mice. Methods: ICR mice were randomly divided into normal group (NC)， model group (ET)， camel milk group (CM) and camel milk intervention group (ET+CM)， and measured liver tissue (AST and ALT) and serum indexes (TNF-α， IL-10， 1L-6 and IL-1β) to reflect the protective effect of camel milk on the liver； and based on transcriptomics research methods to explore the mechanism of camel milk to protect the liver. Results: Compared with the ET group， camel milk intervention reduced the alcohol-induced AST， ALT， TNF-α， 1L-6 and IL-1β levels， and at the same time increased IL-10 levels. Furthermore， transcriptome sequencing was performed on four groups of mouse liver tissues. The results showed that a total of 1426 differentially expressed genes were detected in the ET group and the ET+CM group (673 were up-regulated genes and 753 were down-regulated genes)， and then combined with gene function and enrichment analysis， it was found that the differentially expressed genes were mainly significantly enriched In the three inflammatory pathways of MAPK， Toll-like and NF-κB signaling. Six representative differential genes， including CD14， TLR5 and TLR9， were determined by real-time fluorescence quantitative PCR. The results showed that compared with the model group， the expression levels of CD14， IL-1β， IL-6， TLR5 and TLR9 were significantly decreased after camel milk intervention， and the expression levels of IL-10 were significantly increased， which was consistent with the transcriptomic sequencing results， and verified the accuracy of sequencing data. The results laid a good foundation for the analysis of the molecular mechanism of camel milk on alcoholic liver injury.