Ulcerative colitis (UC) is a major inflammatory disease worldwide. We previously demonstrated that licorice residue flavones (LFs) showed satisfactory efficacy in the treatment of UC. Therefore, research into the ingredients of LFs may lead to the discovery of novel anti-UC targets. In the current study, we separated licoflavone B (LB) from LFs and administered it to dextran sodium sulfate (DSS)-exposed C57BL/6 mice for 14 days. Our results demonstrated that high dose LB (120 mg/kg) significantly prevented DSS-induced weight loss, disease activity index (DAI) increase, histological damage, and colonic inflammation, indicating that LB has ameliorative effects on UC. We also investigated the composition of the intestinal barrier and microflora in an attempt to explore the mechanisms of LB against UC. As a result, we found that LB preserved the integrity of the colonic barrier by inhibiting colonic cell apoptosis and protecting the expression of occludin, claudin-1, and ZO-1. Moreover, LB reshaped the microflora composition by suppressing harmful bacteria (Enterococcus et al.) and boosting beneficial microorganisms (Bacteroides et al.). Further molecular exploration implied that LB exerted anti-UC activity through blocking the MAPK pathway. Here, we explored anti-UC activity of LB for the first time and clarified its mechanisms. These results will provide valuable clues for the discovery of novel anti-UC agents.

溃疡性结肠炎 (UC) 是世界范围内的主要炎症性疾病。我们之前证明了甘草渣黄酮 (LFs) 在治疗 UC 中显示出令人满意的疗效。因此，对LFs成分的研究可能会导致发现新的抗UC靶点。在目前的研究中，我们将甘草黄酮 B (LB) 从 LF 中分离出来，并将其施用于葡聚糖硫酸钠 (DSS) 暴露的 C57BL/6 小鼠 14 天。我们的研究结果表明，高剂量 LB (120 mg/kg) 可显着预防 DSS 引起的体重减轻、疾病活动指数 (DAI) 增加、组织学损伤和结肠炎症，表明 LB 对 UC 具有改善作用。我们还研究了肠道屏障和微生物群落的组成，试图探索 LB 对抗 UC 的机制。因此，我们发现LB通过抑制结肠细胞凋亡和保护occludin、claudin-1和ZO-1的表达来保持结肠屏障的完整性。此外，LB通过抑制有害细菌重塑了微生物群落组成（肠球菌等）和促进有益微生物（拟杆菌等）。进一步的分子探索暗示LB通过阻断MAPK途径发挥抗UC活性。在这里，我们首次探索了LB的抗UC活性并阐明了其机制。这些结果将为发现新型抗UC药物提供有价值的线索。