Intestinal epithelial immune dysfunction or imbalance in the homeostasis of intestinal flora can lead to the occurrence or exacerbation of ulcerative colitis (UC). Prim-O-glucosylcimifugin (POG) is an extract of Chinese traditional medicine (TCM) Saposhnikov, which has analgesic, anti-inflammatory, and antioxidant effects. The present work discussed how the POG alternated ulcerative colitis (UC) along with its underlying mechanism. This was clarified by performing animal studies in a mice model, wherein UC was induced by dextran sulfate sodium (DSS). In vivo studies have found that POG increased clinical score, colonic length, and weight of mice in the ulcerative colitis model. It repaired the pathological injury of an intestinal mucosa within mice while inhibiting the inflammatory factor levels such as IL-1β, TNF-α, and IL-6. Meanwhile, by16SrDNA sequencing analysis, it was found that POG regulated the richness of intestinal microbiota structure and repaired the intestinal immune barrier by upregulating the expression levels of tight junction proteins Occludin, Claudin-3, and ZO-1. To further confirm the above results, we found in in vitro studies that POG also protected lipopolysaccharide- (LPS-) induced RAW264.7 cells. POG dramatically suppressed inflammatory factor production (including TNF-α, IL-1β, and IL-6) within LPS-treated RAW264.7 cells by inhibiting the activation of ERK1/2, AKT, JNK1/2, IκB-α, P38, and P65 phosphorylation. In conclusion, POG plays a protective role against UC by inhibiting the activation of pro-inflammatory signaling pathways MAPK, AKT, and NF-κB; repairing the integrity of the intestinal barrier; and regulating the diversity and abundance of intestinal flora.

肠道上皮免疫功能障碍或肠道菌群稳态失衡可导致溃疡性结肠炎（UC）的发生或加重。Prim-O-glucosylcimifugin (POG) 是中药 (TCM) Saposhnikov 的提取物，具有镇痛、抗炎和抗氧化作用。目前的工作讨论了 POG 如何交替溃疡性结肠炎 (UC) 及其潜在机制。这通过在小鼠模型中进行动物研究得到澄清，其中 UC 是由硫酸葡聚糖钠 (DSS) 诱导的。体内研究发现，在溃疡性结肠炎模型中，POG 增加了小鼠的临床评分、结肠长度和体重。它修复了小鼠肠黏膜的病理损伤，同时抑制了IL-1β、TNF-α和IL-6等炎症因子的水平。同时，通过16SrDNA测序分析发现，POG通过上调紧密连接蛋白Occludin、Claudin-3和ZO-1的表达水平来调节肠道菌群结构的丰富度，修复肠道免疫屏障。为了进一步证实上述结果，我们发现体外研究表明，POG 还保护脂多糖 (LPS-) 诱导的 RAW264.7 细胞。POG 通过抑制 ERK1/2、AKT、JNK1/2、IκB-α、P38、和 P65 磷酸化。总之，POG 通过抑制促炎信号通路 MAPK、AKT 和 NF-κB 的激活对 UC 起保护作用；修复肠道屏障的完整性；调节肠道菌群的多样性和丰度。