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

Yu-Hsing Lin 1, #, Yun-Xuan Chang 2, #, Tzu-Yun Chi 2, #, Tsung-Han Wu 2, #, Ya-Peng Wang 2, Yen-Jung Lu 2, Chia-Yu Lin 2, Ping-Min Huang 2, Guan-Hong Chen 2, Chien-Chao Chiu 2, Ching-Feng Chiu 3, Hsuan-Wen Chiu 4, Wei-Huang Tsai 5, Chia-Chi Chen 2, *, and Shao-Wen Hung 2, 6, *

1 Department of Pet Healthcare, College of Medical Technology and Nursing, Yuanpei University of Medical Technology, Xiangshan, Hsinchu 300, Taiwan.
2 Division of Animal Industry, Animal Technology Research Center, Agricultural Technology Research Institute, Xiangshan, Hsinchu 300, Taiwan.
3 Graduate Institute of Metabolism and Obesity Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan.
4 Department of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan.
5 Department of Science and Technology, Council of Agriculture, Executive Yuan, Taipei 100, Taiwan.
6 Department of Nursing, Yuanpei University of Medical Technology, Hsinchu 300, Taiwan.
# Equally distributed authors.
 
Research Article
International Journal of Frontiers in Life Science Research, 2022, 03(01), 030–038.
Article DOI: 10.53294/ijflsr.2022.3.1.0051
Publication history: 
Received on 30 June 2022; revised on 06 August 2022; accepted on 08 August 2022
 
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.
 
Keywords: 
Establishment of Experimental Mouse Model; Inflammatory Bowel Diseases; Dextran Sulfate Sodium; Ulcerative Disease
 
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