Animal models play critical roles in exploring the pathogenesis of human diseases and designing novel therapeutic schemes. Acute experimental colitis (AEC) models have been reported to be established in mice principally by oral administration of dextran sulfate sodium (DSS). However, little knowledge is known about whether DSS can be used to induce the acute experimental enteritis (AEE). In this study, different concentrations of DSS (0%, 2%, 3%, and 5%) were used to induce AEC and AEE models in two cohorts. After the establishment of these two models, the symptoms of the mice induced by DSS were noted, the length and average weight of each colon and small intestine were measured, and hematoxylin and eosin (HE) staining was conducted for assessing the inflammatory infiltration in these models. Generally, the comparison of the inflammatory scoring between AEC and AEE models was analyzed. As a consequence, we found that, the mice with 2%–5% DSS administration in a week could develop into AEC models in two cohorts and AEE models in one cohort, followed by the signs of diarrhea, gross rectal bleeding, weight loss of the body, and shortened colon and intestine length, as compared with the control group. HE staining showed that the inflammatory scoring was dramatically increased by 3%–5% DSS in AEC models in two cohorts but slightly elevated in AEE models in one cohort. Meanwhile, as compared with the severe AEC models, the extent of inflammatory infiltration induced by 3%–5% DSS in AEE models was much milder. In conclusion, oral administration of 3%–5% DSS is a good inducer of AEC models, but not AEE models.
Oral administration of the anti-proliferative substance taurolidine has no impact on dextran sulfate sodium-induced colitis-associated carcinogenesis in mice
