Objective The aim of this study was to explore the establishment method of an animal model of irritable bowel syndrome (IBS) and the evaluation of this animal model. Methods 30 adult SD rats were randomly divided into two groups: acetic acid irritation and bondage stress group (n=10),bondage stress group (n=10),and normal control group (n=10). The rats of the intervention group received an intra-colonic infusion of 0.4% acetic acid irritation combined with bondage stress to establish an animal model of IBS. The colonic sensitivity of the intervention group rats was assessed by stool test and colorectal distension (CRD) test. Hydrochloric acid toluidine blue staining was used to observe the number degranulation phenomenon of mast cells in the ileocecum. Results On the 7th day, the number of soft feces was 8 and loose stool was 4 in the model group, significantly higher than that in the bondage stress group(0 and 0) (P<0.05),and normal control group (1 and 0) (P<0.05). On the 10th day, when the AWR=2, the average rectal distension volume was 1.2 mL, significantly lower than that in the bondage stress group(1.37mL) (P<0.05),also significantly lower than in the normal control group (1.49 mL) (P<0.05), and when the AWR=4, the average rectal distension volume was 1.49 mL, significantly lower than that in the bondage stress group(1.74mL) (P<0.05),and the normal control group (1.77 mL) (P<0.05). These results indicated that the visceral sensitivity of the model group was significantly higher than that in the bondage stress group and normal control group. Histological analysis showed that the rats of all groups had no obvious inflammatory changes. Conclusions Chronic bondage stress combined with intra-colonic infusion of 0.4% acetic acid irritation can be used to increase the visceral sensitivity and amount and degranulation of mast cells in the intestinal tissue in rats. This established rat model shows pathogenetic changes resembling the pathogenesis of human irritable bowel syndrome, and provides a useful animal model for further studies of the pathogenesis of this disease.