School of Food and Biological Engineering, Hefei University of Technology, Hefei, 230009, China.
Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, Hefei, 230009, China.
Food Funct. 2022 Jan 4;13(1):143-160. doi: 10.1039/d1fo03003e.
The ameliorative effect of polysaccharide (cDFPW1) on ulcerative colitis (UC) was investigated using a dextran-sodium-sulfate-induced (DSS-induced) mouse model in the present study. The results showed that cDFPW1 effectively improved colitis in mice by ameliorating weight loss, disease activity index (DAI) and colonic pathological damage, and by protecting the intestinal barrier function integrity. Moreover, cDFPW1 modulated the composition and metabolism of intestinal microbiota through enhancing , and , and reducing , and in colitis mice. Notably, cDFPW1 significantly restored the homeostasis of Th17/regulatory T (Treg) cells and the expression of specific cytokines. Western blotting of colon tissues showed that cDFPW1 markedly up-regulated the expression of Nrf2 and inhibited the phosphorylation of NF-κB signaling. These results indicated that cDFPW1 possesses the potential of improving UC and its effect on palliating colitis may be connected with the regulation of Nrf2/NF-κB signaling.
本研究采用葡聚糖硫酸钠（DSS）诱导的小鼠模型探讨了多糖（cDFPW1）对溃疡性结肠炎（UC）的改善作用。结果表明，cDFPW1 通过改善体重减轻、疾病活动指数（DAI）和结肠病理损伤，以及保护肠道屏障功能完整性，有效改善了小鼠的结肠炎。此外，cDFPW1 通过增强和，降低和，调节肠道微生物群落的组成和代谢。值得注意的是，cDFPW1 显著恢复了 Th17/调节性 T（Treg）细胞的平衡和特定细胞因子的表达。结肠组织的 Western 印迹表明，cDFPW1 显著上调了 Nrf2 的表达并抑制了 NF-κB 信号的磷酸化。这些结果表明，cDFPW1 具有改善 UC 的潜力，其缓解结肠炎的作用可能与调节 Nrf2/NF-κB 信号有关。
