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Publication
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| Research Title |
A dextran sulfate sodium-induced ulcerative colitis in ICR mouse model |
| Date of Distribution |
8 March 2019 |
| Conference |
| Title of the Conference |
35th International Annual Meeting in Pharmaceutical Sciences (IAMPS35) |
| Organiser |
Faculty of Pharmaceutical Sciences, Chulalongkorn University |
| Conference Place |
Eastin hotel, Makkasan |
| Province/State |
Bangkok |
| Conference Date |
8 March 2019 |
| To |
8 March 2019 |
| Proceeding Paper |
| Volume |
- |
| Issue |
- |
| Page |
103 |
| Editors/edition/publisher |
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| Abstract |
Ulcerative colitis is an idiopathic inflammatory disease. Due to uncertain etiology of UC, an experimental animal colitis model has been developed to study pathophysiological mechanism of the disease. Dextran sulfate sodium (DSS)-induced UC model is one of the most common models. However, there were few reports of DSS-induced UC in an outbred mouse strain. This study aimed to examine impact of DSS to induce UC in ICR mice. DSS (40 kDa) solution (21% w/v in sterile water) was prepared. Five-week-old male ICR mice were given a 0.25 mL-aliquot of DSS solution 4 times per day by gastric lavage tube for 4 and 7 consecutive days. The control group was simply given sterile water. Disease activity index (DAI), by which calculation is based on body weight loss, stool consistency, and visible blood in feces, was daily recorded. At the end of the study, the mice were euthanized and their colons were collected to examine histomorphology by hematoxylin and eosin staining. Severity of the disease was indicated by increment of the DAI score. DSS-treated group extensively demonstrated a daily DAI score increase. After 4 and 7 days of the induction, colon was significantly shortened when compared with the control; this was classified as an indirect marker of inflammation in DSS-induced mice. On the day 4 of induction, the DSS-treated mice showed histological changes include goblet cell depletion, crypt of Lieberkühn damage, and epithelial erosion. Moreover, DSS induced an infiltration of inflammatory cells to mucosa layer. Interestingly, on the 7-day-induction goblet cells and the crypt were not observed, followed by severe epithelial erosion and ulceration. These findings assure the potential of an ICR mouse strain to develop as a DSS-induced UC model which is of interest for further investigating the underlying pathophysiological mechanisms of UC. |
| Author |
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| Peer Review Status |
มีผู้ประเมินอิสระ |
| Level of Conference |
นานาชาติ |
| Type of Proceeding |
Abstract |
| Type of Presentation |
Poster |
| Part of thesis |
true |
| Presentation awarding |
false |
| Attach file |
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| Citation |
0
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Journal Publication
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