Carboxyamidotriazole ameliorates experimental colitis by inhibition of cytokine production, nuclear factor-κB activation, and colonic fibrosis

The Journal of Pharmacology and Experimental Therapeutics
Lei GuoDechang Zhang

Abstract

Carboxyamidotrizole (CAI) has been reported to suppress the production of tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β and be effective in rats with adjuvant arthritis. The aim of this study was to investigate the role of CAI in inflammatory bowel disease (IBD). We assessed the effect of CAI in dextran sodium sulfate-induced colitis. Inflammation was scored histologically, and potential mediators of IBD were assessed by immunohistochemical and molecular biochemical approaches. CAI-treated colitis animals revealed much fewer signs of colitis with significantly decreased macroscopic and microscopic scores than vehicle-treated animals. CAI inhibited the production of TNF-α, IL-1β, and IL-6 in serum, supernatant of peritoneal macrophages, and lamina propria. CAI also decreased the expression of intercellular adhesion molecule-1 in colonic tissues. Furthermore, CAI prevented nuclear factor-κB (NF-κB) activation and inhibitor of nuclear factor-κBα phosphorylation and degradation. In addition, CAI showed a beneficial effect on colonic fibrosis, possibly by reducing the production of the fibrogenic cytokine transforming growth factor-β. The results support that CAI administration is effective in ameliorating experimental col...Continue Reading

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Citations

Jan 27, 2017·Naunyn-Schmiedeberg's Archives of Pharmacology·Chen ChenLei Guo
Sep 13, 2019·Journal for Immunotherapy of Cancer·Jing ShiDechang Zhang
Dec 5, 2020·The EMBO Journal·Jiadi LvBo Huang
May 4, 2021·Frontiers in Cell and Developmental Biology·Heba ShawerMarc A Bailey

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