The aim of this study was to evaluate the effect of fexofenadine on intestinal inflammation. Fexofenadine significantly inhibited the upregulated expression of interleukin-8 (IL-8) in HCT116 and COLO205 cells stimulated with tumor necrosis factor-α. Fexofenadine suppressed nuclear factor-κB DNA-binding activity. In addition, the induction of endoplasmic reticulum stress markers, caspase-12 and p-eukaryotic initiation factor (eIF2)-α, was significantly suppressed by the pretreatment of fexofenadine. Administration of fexofenadine significantly reduced the severity of dextran sulfate sodium (DSS)–induced murine colitis, as assessed by the disease activity index, colon length, and histology. In addition, the DSS-induced phospho-IκB kinase activation was significantly decreased in fexofenadine-pretreated mice. Finally, fexofenadine significantly reduced the severity of colitis and the immunoreactivity of caspase-12 and p-eIF2-α in IL-10−/− mice. These results suggest that fexofenadine is a potential therapeutic agent for the treatment of inflammatory bowel disease.
See article at J Pharmacol Exp Ther 2015, 352:455–461.
- Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics