Objective： To explore the protective effect of ursolic acid （UA） on intestinal mucosal barrier injury in alcohol-induced rats. Methods： SD rats were randomly divided into 4 group. Rats of normal control group received physiological saline by gavage for every day. Rats of alcohol model group were given oral dose of 8 mL/（kg bw·d） of 50% alcohol for the first to the second week， a dose of 12 mL/（kg bw·d） from the third week. Ursolic acid group were administered orally with 150 mg/（kg bw·d） UA for every day and received alcohol by gavage 1 hour later. Glutamine group were given 300 mg/（kg bw·d） glutamine by gavage for every day and the alcohol dose was the same as that of ursolic acid group. After 8 weeks， morphological examination of intestinal tissue was performed by hematoxylin and eosin （H&E） staining， and the ultrastructure of intestinal mucosal was observed by transmission electron microscopy. The levels of D-lactic acid （D-LA）， intestinal fatty acid binding protein （FABP2）， tumor necrosis factor alpha （TNF-α） and interleukin 1 beta （IL-1β） in plasma were detected. The expressions of forkhead box O4 （FOXO4）， p-FOXO4， and zonula occludens-1（ZO-1） in intestinal tissues were detected. Results： The morphological structure and the ultrastructure of intestinal tissues showed the villi of the rats in the alcohol model group were atrophic and short， the tight junction were swelling and the inflammatory cell infiltration was obvious. The pathological changes of small intestine mucosa in the ursolic acid group and glutamine group were better than alcohol model group. Plasma concentrations of D-LA， FABP2， TNF-α and IL-1β were significantly decreased. The expression of p-FOXO4 was decreased， ZO-1 was increased compared model group. There was no significant difference in FOXO4 expression. Conclusion： UA attenuates the damage of intestinal mucosal barrier injury caused by alcohol in rats， and its mechanism may be related to improving intestinal mucosal permeability， inhibiting the phosphorylation of FOXO4 protein， and thereby reducing the release of pro-inflammatory factors TNF-α and IL-1β.