Herbacetin

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.