1. Citropten alleviates acute and recurrent colitis via blockage of NF-κB and JAK/STAT3 pathways.
- Author
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Tang YZ, Liu Y, Chen YP, Feng TT, Liu YY, Wang Y, Zhang JP, and Xu WH
- Subjects
- Animals, Mice, Colon pathology, Coumarins pharmacology, Coumarins therapeutic use, Disease Models, Animal, Inflammation metabolism, Inflammation Mediators metabolism, Mice, Inbred C57BL, NF-kappa B metabolism, Colitis chemically induced, Colitis drug therapy, Colitis metabolism, Inflammatory Bowel Diseases pathology
- Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory bowel disease, which is characterized by inflammation, with many symptoms including diarrhea, abdominal pain, bloody stool, and weight loss. It is difficult to completely cure and promising therapeutic drug candidates are urgently needed. Citropten, a coumarin-like compound found in traditional Chinese medicine such as Finger Citron Fruit, notopterygium root and citrus peel, has been shown to inhibit the proliferation of tumor cells, protect against depression and suppress the production of inflammatory mediators. In this study, we demonstrated that citropten could alleviate dextran sulfate sodium (DSS)-induced acute and recurrent colitis in mice, with significant improvement in body weight loss, disease activity index, shortened colon length and histological changes. Moreover, citropten dramatically decreased the production of pro-inflammatory mediators in colon tissues and effectively suppressed the proportion of Th17 cells in spleen. Mechanism investigations revealed that citropten significantly inhibited the activation of NF-κB and JAK/STAT3 signaling pathways, thus leading to decreased inflammation, Th17 cells and alleviative colitis. These findings provide novel insights into the anti-colitis effect of citropten, which may be a promising drug candidate for treatment of IBD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)
- Published
- 2023
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