Anti‐ulcerative effects of wogonin on ulcerative colitis induced by dextran sulfate sodium via Nrf2/TLR4/NF‐κB signaling pathway in BALB/c mice

Abstract Ulcerative colitis (UC) is an inflammatory disease on the deepest lining of the colon and rectum. Wogonin is an antitumor flavonoid, which possesses various therapeutic properties. Even if the anti‐colitis effect of wogonin was documented earlier, but the wogonin effect on inflammation underlying mechanism is not fully elucidated. In this present study, we hypothesized to study the oxidative damage, anti‐inflammatory, and molecular action of wogonin on dextran sulfate sodium (DSS)‐induced UC mice model. In methods, mice were categorized into four groups: that is, normal control, DSS alone, DSS + wogonin (30 mg/kg/day), and DSS + sulfasalazine (50 mg/kg/day). We determined the biochemical markers, inflammatory cytokines, histopathology of colon tissue, and western blot analysis. DSS significantly reduced body weight, colon length, and increased inflammation in the colon. Wogonin treatment prevented colonic ulceration, neutrophil infiltration, oxidative stress, pro‐inflammatory cytokines, and histological changes. Oxidative damage and inflammatory mediators' elevation were also dramatically diminished by wogonin. Wogonin activates apoptosis via inhibiting Bcl‐2 and augmenting Bax, caspase‐3, and ‐9 expressions. Wogonin downregulated the COX‐2 and iNOS, thereby repressing NF‐κB. Wogonin regulated the Nrf2 signaling pathway and decreased TLR‐4/NF‐κB triggering. Taken together our study exposed that wogonin has a promising anti‐ulcerative agent and recommended for good anti‐inflammatory drug in the colon.