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.

中文翻译：

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大豆苷元通过调节NF-κB信号传导改善小鼠的葡聚糖硫酸钠诱导的实验性结肠炎。

溃疡性结肠炎（UC）和克罗恩氏病（CD）统称为炎性肠病（IBDs）。UC的发病机制增加导致一系列并发症。我们旨在分析大豆苷元（DA）在右旋糖酐硫酸钠（DSS）诱导的结肠炎小鼠模型和活化的巨噬细胞RAW264.7细胞中的防龋作用。将30只BALB / c雄性小鼠随机分为三组：对照组，DSS治疗组和DSS DA（10 mg / kg体重，持续7天）。发现补充DA可改善疾病活动指数，结肠长度和脾脏重量。显微镜分析显示，DSS诱导的小鼠在绒毛中显示出更多的炎性细胞浸润和侵蚀。补充DA可显着减少这些症状。此外，口服DA可降低髓过氧化物酶（MPO）的水平，并抑制p65-NF-κB，p-IκB-α和p-IKK的表达以及多种炎症因子，包括TNF-α，IL-1β和IL-6，在结肠组织中。DA还抑制LPS刺激的RAW 264.7巨噬细胞中一氧化氮和前列腺素E2的产生。两者合计，这些结果表明DA可以抑制DSS诱导的溃疡性结肠炎并降低炎症因子的表达。因此，DA可能适用于UC的治疗。这些结果表明，DA可以抑制DSS诱导的溃疡性结肠炎并降低炎症因子的表达。因此，DA可能适用于UC的治疗。这些结果表明，DA可以抑制DSS诱导的溃疡性结肠炎并降低炎症因子的表达。因此，DA可能适用于UC的治疗。