miRNA-133a-UCP2 pathway regulates inflammatory bowel disease progress by influencing inflammation, oxidative stress and energy metabolism

作者：Xi Jin, Dong Chen, Ruoheng Zheng, Hong Zhang, Yi-Peng Chen, Zun Xiang · 发表于：World Journal of Gastroenterology · 年份：2017 · DOI：10.3748/wjg.v23.i1.76 · 被引用次数：61 · 研究领域：MicroRNA in disease regulation、Inflammasome and immune disorders、Inflammatory Bowel Disease

AIM: To investigate the role of the miR-133a-UCP2 pathway in the pathogenesis of inflammatory bowel disease (IBD) and to explore the potential downstream mechanisms with respect to inflammation, oxidative stress and energy metabolism. METHODS: and MDA) and metabolic parameters (ATP) by ELISA and colorimetric methods. RESULTS: An animal model of IBD was successfully established, as shown by an increased DAI score, shortened colon length and specific pathologic changes, along with significantly increased UCP2 and decreased miR-133a levels. Compared with the DSS group, the severity of IBD was alleviated in the UCP2 and the miR-133a groups after successful UCP2 knockdown and miR-133a overexpression. The extent of apoptosis, as well as the levels of TNF-α, IL-1β, MDA and ATP, were significantly increased in both the UCP2 and miR-133a groups compared with the DSS group. CONCLUSION: The miR-133a-UCP2 pathway participates in IBD by altering downstream inflammation, oxidative stress and markers of energy metabolism, which provides novel clues and potential therapeutic targets for IBD.