ABSTRACT Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) resulting from a dysregulation of immune responses. Herbacetin, a flavonoid of natural origin, has been found to exert an anti‐inflammatory action, though its actions in experimental colitis are unknown. Colitis was induced in BALB/c mice with 2,4,6‐trinitrobenzenesulfonic acid (TNBS). Mice were administered with herbacetin (25, 50, 100 mg/kg) or sulfasalazine (100 mg/kg) orally for 7 days. The disease activity index (DAI), colon length, weight/length ratio, histopathology, MPO and NO contents, and inflammatory gene expression (NF‐κB, iNOS, COX‐2, NLRP3, IL‐1β, IL‐18) were evaluated. TNBS induced marked weight loss and increased DAI ( p < 0.01 vs. NC). Body weight ( p < 0.01) and DAI ( p < 0.01) were significantly ameliorated by herbacetin, especially at 50 and 100 mg/kg. TNBS significantly reduced the colon length ( p < 0.001) and increased the weight/length ratio ( p < 0.001), which were significantly counteracted by herbacetin ( p < 0.01–0.001). TNBS mice presented with mucosal injury and inflammatory infiltration were demonstrated by histopathology ( p < 0.001) and a dose‐dependent healing effect was observed in herbacetin‐treated mice. TNBS mice had higher levels of MPO and NO ( p < 0.001), which were significantly attenuated by herbacetin ( p < 0.01–0.001). Herbacetin decreased the mRNA expression levels of NF‐κB, iNOS, COX‐2, NLRP3, IL‐1β, and IL‐18 in a dose‐dependent ( p < 0.05–0.001). Herbacetin exerts a protective effect in colitis by suppressing neutrophil infiltration, oxidative stress, and NF‐κB–NLRP3‐mediated inflammation, highlighting the potential of herbacetin‐based treatment for UC and related inflammatory bowel diseases.
Bseiso et al. (Sun,) studied this question.