Abstract：
Ulcerative colitis (UC) is one of the most prevalent inflammatory bowel diseases and poses a serious threat to human health. Currently, safe and effective preventive measures are unavailable. In this study, the protective effects of asiaticoside (AS) on dextran sodium sulfate (DSS)-induced colitis in mice and the underlying molecular mechanism were investigated. In this experiment, colitis was induced in mice with DSS. Subsequently, the role of AS in colitis and its underlying mechanisms were examined using H&E staining, immunofluorescence staining, western blot, Elisa, FMT, and other assays. The results showed that AS significantly attenuated the related symptoms of DSS-induced colitis in mice. In addition, AS inhibited the activation of signaling pathways TLR4/NF-κB and MAPK reduced the release of inflammatory factors, thereby attenuating the inflammatory response in mice. AS administration also restored the permeability of the intestinal barrier by increasing the levels of tight junction-associated proteins (claudin-3, occludin, and ZO-1). In addition, AS rebalanced the intestinal flora of DSS-treated mice by increasing the diversity of the flora. AS can alleviate DSS-induced ulcerative colitis in mice by maintaining the intestinal barrier, thus inhibiting the signaling pathways TLR4/NF-κB and MAPK activation, reducing the release of inflammatory factors, and regulating intestinal microecology.
摘要：
溃疡性结肠炎(ulcerativecolitis,UC)是最常见的炎症性肠病之一,严重威胁人类健康。目前,缺乏安全有效的预防措施。在这项研究中,研究积雪草苷（AS）对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的保护作用及其分子机制。在这个实验中,在具有DSS的小鼠中诱导结肠炎。随后，使用H&E染色检查AS在结肠炎中的作用及其潜在机制，免疫荧光染色，westernblot,Elisa,FMT,和其他化验。结果表明，AS可显著减轻DSS诱导小鼠结肠炎的相关症状。此外,AS抑制TLR4/NF-κB和MAPK信号通路的激活，减少炎症因子的释放，从而减弱小鼠的炎症反应。AS给药还通过增加紧密连接相关蛋白（claudin-3，occludin，和ZO-1）。此外,AS通过增加菌群的多样性来重新平衡DSS处理的小鼠的肠道菌群。AS可以通过维持肠道屏障缓解DSS诱导的小鼠溃疡性结肠炎,从而抑制信号通路TLR4/NF-κB和MAPK的激活,减少炎症因子的释放，调节肠道微生态。
