溃疡性结肠炎(UC)是一种以炎症失衡为特征的慢性炎症性肠病,肠上皮粘膜损伤,和肠道微生物群的生态失调。黄精多糖(PCPs)可以调节肠道菌群和炎症。这里,将不同剂量的PCPs给予葡聚糖硫酸钠诱导的UC小鼠,并将整个PCP的作用与分馏的PCP-1(19.9kDa)和PCP-2(71.6和4.2kDa)的作用进行了比较。此外,对UC小鼠施用抗生素混合物以消耗肠道微生物群,随后施用PCP以阐明肠道微生物群在这些小鼠中的潜在作用。结果表明,PCP治疗显着优化了体重减轻和缩短结肠,恢复了炎症的平衡,减轻氧化应激,并恢复肠上皮粘膜损伤。And,与PCP-1和PCP-2相比,PCP在改善这些症状方面表现出更好的疗效。然而,肠道微生物群的消耗降低了PCPs在UC小鼠中的治疗效果。此外,从PCP处理的UC小鼠的粪便移植到新的UC患病小鼠产生了类似于PCP处理的治疗效果。所以,PCP显著改善了症状,炎症,氧化应激,和UC小鼠的肠粘膜损伤,和肠道微生物群部分介导了这些作用。
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized inflammatory imbalance, intestinal epithelial mucosal damage, and dysbiosis of the gut microbiota. Polygonatum cyrtonema polysaccharides (PCPs) can regulate gut microbiota and inflammation. Here, the different doses of PCPs were administered to dextran sodium sulfate-induced UC mice, and the effects of the whole PCPs were compared with those of the fractionated fractions PCP-1 (19.9 kDa) and PCP-2 (71.6 and 4.2 kDa). Additionally, an antibiotic cocktail was administered to UC mice to deplete the gut microbiota, and PCPs were subsequently administered to elucidate the potential role of the gut microbiota in these mice. The results revealed that PCP treatment significantly optimized the lost weight and shortened colon, restored the balance of inflammation, mitigated oxidative stress, and restored intestinal epithelial mucosal damage. And, the PCPs exhibited superior efficacy in ameliorating these symptoms compared with PCP-1 and PCP-2. However, depletion of the gut microbiota diminished the therapeutic effects of PCPs in UC mice. Furthermore, fecal transplantation from PCP-treated UC mice to new UC-afflicted mice produced therapeutic effects similar to PCP treatment. So, PCPs significantly ameliorated the symptoms, inflammation, oxidative stress, and intestinal mucosal damage in UC mice, and gut microbiota partially mediated these effects.