Daidzein Ameliorates Dextran Sulfate Sodium-Induced Experimental Colitis in Mice by Regulating NF-κB Signaling

Ulcerative colitis (UC) and Crohn's disease (CD) are collectively referred to as inflammatory bowel diseases (IBDs). The increased pathogenesis of UC leads to a series of complications. We aimed to analyze the anticolitic effect of daidzein (DA) in a dextran sulfate sodium (DSS)-induced colitis mouse model and in activated macrophage RAW264.7 cells. Thirty BALB/c male mice were randomly divided into three groups: control, DSS-treated, and DSS DA (10 mg/kg body weight for seven days). DA supplementation was found to improve the disease activity index, colon length, and spleen weight. Microscopic analysis revealed that DSS-induced mice showed more inflammatory cell infiltration and erosion in the villi. Supplementation of DA reduced these signs significantly. Furthermore, oral administration of DA decreased the level of myeloperoxidase (MPO) and inhibited the expression of p65-NF-κB, p-IκB-α, and p-IKK as well as several inflammatory factors, including TNF-α, IL-1β, and IL-6, in the colonic tissues. DA also inhibited the production of nitric oxide and prostaglandin E2 in LPS-stimulated RAW 264.7 macrophages. Taken together, these results suggest that DA could inhibit DSS-induced ulcerative colitis and decrease inflammatory factor expression. Thus, DA might be applicable in the treatment of UC.