Objective To explore the effects and mechanism of Shenqu Xiaoshi oral liquid ( SXOL) on gastrointestinal motility in mice with functional dyspepsia (FD). Methods This study involved 50 KM mice. Ten mice were randomly assigned to the normal group, and the remaining 40 mice were used to establish animal models of FD by the irregular eating and L-arginine method . They were then randomly divided into a model group, low-dose SXOL group, medium-dose SXOL group, and high-dose SXOL group. Routine blood and liver/ kidney function indexes were measured. Their body weight was recorded, gastric residual rate and intestinal propulsion rate were calculated, and pathological changes in gastric tissues were observed. Real-time quantitative polymerase chain reaction and Western blot were used to detect expression of inositol-requiring enzyme 1 (IREl) and tumor necrosis factor receptor-associated factor 2 (TRAF2) in gastric tissues. Results There were no significant differences in the white blood cell count, red blood cell count, hemoglobin concentration, platelet count, lymphocyte count, monocyte count, neutrophil count, aspartate aminotransferase concentration, alanine aminotransferase concentration, total bile acid concentration, blood urea nitrogen concentration, or creatinine concentration among all groups ( P> 0. 05). The structure of the gastric mucosal layer, submucosal layer, muscle layer, and serosal layer in each group was clear, and there were no obvious pathological changes. Compared with the model group, the gastric emptying rate and small intestinal propulsion rate were significantly higher in the low-dose, medium-dose, and high-dose SXOL groups, while expression of IREl and TRAF2 mRNA and protein was significantly decreased in gastric tissues (P< 0. 05). Conclusions SXOL has no significant effects on routine blood and liver/ kidney function indices in normal mice. However, SXOL can significantly improve gastrointestinal motility function in mice with FD, which may be related to down-regulation of the expression of the endoplasmic reticulum factors IR11 and TRAF2.