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An experimental model of colitis induced by dextran sulfate sodium from acute progresses to chronicity in C57BL/6: correlation between conditions of mice and the environment

AIM: To induce acute colitis progresses to chronicity in C57BL/6 mice by dextran sulfate sodium. BACKGROUND: Murine models are essential tools to understand IBD pathogenesis. Among different types of chemically induced colitis models, the dextran sulfate sodium (DSS)-induced colitis model is the mos...

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Detalles Bibliográficos
Autores principales: Taghipour, Niloofar, Molaei, Mahsa, Mosaffa, Nariman, Rostami-Nejad, Mohammad, Asadzadeh Aghdaei, Hamid, Anissian, Ali, Azimzadeh, Pedram, Zali, Mohammad Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4702041/
https://www.ncbi.nlm.nih.gov/pubmed/26744614
Descripción
Sumario:AIM: To induce acute colitis progresses to chronicity in C57BL/6 mice by dextran sulfate sodium. BACKGROUND: Murine models are essential tools to understand IBD pathogenesis. Among different types of chemically induced colitis models, the dextran sulfate sodium (DSS)-induced colitis model is the most common model of IBD, due to its simplicity. PATIENTS AND METHODS: Male C57BL/6 mice 6–8 weeks old, were collected and matched by age with controls. C57BL/6 mice treated with 2 cycles of 3.5% DSS for 4 days and 4 days of pure water between each cycle. After that, mice were sacrificed and the entire colon was removed. Small sections of the colon were fixed in formaldehyde, embedded in paraffin and sectioned with a microtome. Sections were stained with hematoxylin eosin to analyses the degree of inflammation. RESULTS: After the first cycle oral administration of DSS, mice with severe and visible rectal bleeding and diarrhea entered into the acute phase. After day 4-5, bleeding and diarrhea were improved and mice entered into the chronic phase with peak levels of weight loss. Macroscopically, the inflammation was predominantly located in the distal colon. Microscopically, examination of the distal colon sections showed a decrease number of goblet cells, loss of crypts, signs of surface epithelial regeneration and moderate to severe infiltration of inflammatory cells in the mucosa. CONCLUSION: In order to achieve an experimental colitis model, our protocol is recommended for future therapies in IBD experimental modeling.