Abstract: OBJECTIVE To investigate the changes of mucosal inflammatory factors, stress status and their Wnt5a/β-catenin signaling pathway in rats with bacterial peritonitis. METHODS The bacterial peritonitis model was established in rats, and rats with successful experimental bacterial peritonitis were divided into 8 h, 16 h and 24 h model groups, with 10 rats in each group. The changes in physical signs and serum endotoxin of the rats in each group were detected at 8 h, 16 h, and 24 h after the injection of the bacterial solution, the pathological changes of the peritoneal mucosa were observed, and the expression levels of mucosal inflammatory factors IL-1β, IL-4, IL-6, IL-10 and TNF-α, and the levels of stress factors SOD, MDA, GSH-Px and ROS, as well as Wnt5a/β-catenin signaling pathway-related proteins and mRNA levels in mucosal tissue were detected. RESULTS The DAI assessment and endotoxin level in the control group were lower than those in the model group; the mucosal structure of rats in the control group was clear, and there was no congestion, edema, and inflammatory infiltration, while the mucosal epithelial cells in the model group had significant necrosis and detachment, edema, hemorrhage, and massive inflammatory cell infiltration; the expression levels of IL-1β, IL-4, IL-6 and TNF-α in the model group were higher than those in the control group, while the expression level of IL-10 was lower than that in the control group (P<0.001); the levels of MDA and ROS in the model group were higher than those in the control group, and the levels of SOD and GSH-Px were lower than those in the control group (P＜0.001); the expression of Wnt5a/β-catenin protein and mRNA in the model group were higher than those in the control group (P＜0.001). CONCLUSION The Wnt5a/β-catenin signaling pathway was associated with mucosal inflammation and stress state in rats with bacterial peritonitis, and its mechanism of initiation might be the activation of inflammatory cells to release IL-1β, IL-6 and TNF-α induced by Wnt5a/β-catenin, and decrease the release of anti-inflammatory factor IL-10, which in turn mediated stress damage to the mucosa.