Date of Award

2015

Document Type

Open Access Thesis

Department

Exercise Science

Sub-Department

Norman J. Arnold School of Public Health

First Advisor

Raja Fayad

Abstract

Background: Acute Dextran Sodium Sulfate (DSS)-induced colitis is an inflammatory ailment limited to the colon. It works to destroy the morphology and gut barrier goblet and epithelial cells that aid in providing homeostasis. Selenium (Se) is an essential micronutrient that has anti-inflammatory and antioxidant properties and is known to play a role in reducing inflammation in areas elsewhere in the body. The current study is focused on how Se alters gut barrier permeability and functionality related to the recovery of tight junction regulation and mucin secretion. Methods: C57BL/6 mice were randomly placed into control (normal water) and 2% DSS water receiving groups and within these groups they were randomly given either a Se rich diet or a control diet ad libidum. Hemotoxylin-Eosin and Alcian Blue staining was used to study the colon morphology and to quantify the goblet to epithelial cell ratio. Western Blot was used to analyze protein expression levels for MUC-2 and ZO-1. Gut barrier permeability was assessed by administering FD4 and determining its plasma concentration by spectrofluorescence. ELISA was used to study the colon-secreted cytokine levels of TNF-α and IL-1β. Results: DSS + Se mice showed significantly lower clinical scores, histopathology, and higher goblet to epithelial cell ratios compared to DSS mice given a control diet. It is interesting to note that there was a main effect of diet and DSS treatment with ZO-1 expression. We found no significant difference between the groups for gut permeability as well as for MUC-2 expression, and IL-1β or TNF-α secretion. Conclusion: The data suggests that Se works to reduce the severity of colitis by increasing ZO-1 expression and goblet cell content.

Rights

© 2015, Sarah Depaepe

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