背景:溃疡性结肠炎(UC),慢性炎症性胃肠病,在世界范围内变得越来越普遍。麦冬素D,来源于麦冬,具有抗炎和抗氧化特性,然而其在UC中的治疗潜力仍不清楚.
方法:在本研究中,我们采用DSS诱导的结肠炎小鼠模型来评估麦冬苷D对各种参数的影响,包括减肥,血淋淋的凳子,还有结肠的炎症.
结果:麦冬苷-D治疗可显着减轻这些DSS诱导的作用,改善结肠通透性,和调节炎症标志物如ZO-1,MUC-2,TNF-α,与对照组相比,小鼠中的IL-1β。此外,与DSS治疗组相比,麦冬皂甙-D治疗改善了小鼠肠道菌群的α-和β-多样性指数,随着Akkermansia(AKK)等属的丰度增加和肠杆菌等属的丰度减少。值得注意的是,丙酸,AKK的代谢产物,与对照组相比,小鼠DSS诱导的结肠炎症状显着改善。此外,丙酸给药还导致肠组织内炎性因子和钙网蛋白水平的改变。
结论:总体而言,麦冬皂甙D显著影响肠道菌群组成,从而改善DSS诱导的小鼠结肠炎的症状。这些发现为溃疡性结肠炎的治疗提供了有希望的治疗策略和潜在的候选药物。
BACKGROUND: Ulcerative colitis (UC), a chronic inflammatory gastrointestinal disorder, is becoming increasingly prevalent worldwide. Ophiopogonin D, which is derived from Ophiopogon japonicus, exhibits anti-inflammatory and antioxidant properties, yet its therapeutic potential in UC remains unclear.
METHODS: In this study, we employed a mouse model of
DSS-induced colitis to assess the impact of Ophiopogonin D on various parameters, including weight loss, bloody stools, and inflammation in the colon.
RESULTS: Ophiopogonin-D treatment significantly mitigated these
DSS-induced effects, improved colon permeability, and modulated inflammatory markers like ZO-1, MUC-2, TNF-α, and IL-1β in mice compared with the control. Furthermore, compared to the
DSS-treatment group, Ophiopogonin-D treatment improved the α- and β-diversity indices of the mouse intestinal microbiota, along with an increase in the abundance of genera such as Akkermansia (AKK) and a decrease in the abundance of genera such as Enterobacter. Notably, propionic acid, a metabolite of AKK, demonstrated significant improvement in the symptoms of
DSS-induced colitis in mice compared to the control. Moreover, propionic-acid administration also resulted in alterations in the levels of inflammatory factors and calreticulin within the intestinal tissues.
CONCLUSIONS: Overall, Ophiopogonin D significantly affects intestinal microbiota composition, thereby improving symptoms of
DSS-induced colitis in mice. These findings present promising therapeutic strategies and potential pharmaceutical candidates for the treatment of ulcerative colitis.