Establishment of a dextran sulfate sodium-induced ulcerative disease mouse model

Abstract

Inflammatory bowel diseases (IBD) are multifactorial chronic intestinal disorders. Currently, mesalamine etc. and therapeutic strategies were suggested for IBD therapy. However, the etiology of IBD remains unclear which is an ongoing challenge and side effects of therapeutic drugs must be also considered. Thus, the aim of this study was to establish an optimal mouse model of IBD for the drug and therapeutic strategy investigations. Herein, 12 mice with 2% dextran sulfate sodium (DSS)-induced colitis (the negative control group) were via oral administration. Twelve mice were administered with drinking water without 2% DSS (the normal control group) via the same method as DSS-induced mice. At the end of the experiment, the body weight (BW), the stool appearance/status, the macroscopic and microscopic colonic injuries, and myeloperoxidase (MPO) activity were monitored, measured, and scored. The results showed that BALB/c mice’ BW decreased on D6-D8 of 2% DSS induction and then BALB/c mice’ BW continuously increased until D13 of the experiment. The stool appearance/status was seen soft stool on D2 of 2% DSS induction. The soft stool was mainly occurred on D2-D6 of 2% DSS induction. In addition, the watery stool was occurred on D4 of 2% DSS induction and was continuous until the end of the experiment (D14). The macroscopic colonic injuries were showed that colon length of the negative group (2% DSS-induced group) was significantly shorter than that of the normal control group (p < 0.001). The colon weight of the negative group was significantly increase than that of the normal control group (p < 0.001). The colon weight / length ratio in the negative group was significantly higher than that of the normal control group (p < 0.001). According to the histopathologic scores (evaluation of the microscopic colonic injuries), the scores of area, ulceration, inflammation, and edema in the colon tissues of the negative group was significantly higher than that of the normal control group (p < 0.001). The total histopathologic scores in the negative group was significantly higher than that of the normal control group (p < 0.001). The myeloperoxidase (MPO) activity in the inflamed colon tissue of the negative group was significantly higher than that of the normal control group (p < 0.001). Taken all results together, a DSS-induced ulcerative disease mouse model was successfully established. We hope that this animal model may be a useful tool for the research of the better therapeutics for IBD.