Inflammatory bowel disease (IBD) has been gradually considered as a public health challenge worldwide. This study determined the protective effect of Lachnum polysaccharide (LEP) on dextran sulfate sodium (DSS)-induced experimental colitis in mice and explored the underlying mechanism. Results showed that dietary LEP reduced DSS-induced disease activity index (DAI), colon shortening and colonic tissue damage. LEP treatment restored intestinal barrier integrity by regulating the expression of tight junction proteins and mucus layer protecting proteins. Moreover, pro-inflammatory cytokine production was inhibited by LEP through regulating PPARγ/NF-κB and IL-6/STAT3 pathways and inhibiting inflammatory cell infiltration. In addition, LEP also inhibited (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation, endoplasmic reticulum (ER) stress and oxidative/nitrosative stress induced by DSS. These results provided a scientific basis for LEP as a potential natural agent for protecting mice from DSS-induced IBD.

中文翻译：

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Lachnum多糖对小鼠右旋糖酐硫酸钠诱导的结肠炎的保护作用。

炎症性肠病（IBD）已逐渐被认为是全球范围内的公共卫生挑战。这项研究确定了Lachnum多糖（LEP）对硫酸葡聚糖钠（DSS）诱导的小鼠实验性结肠炎的保护作用，并探讨了其潜在机制。结果表明，饮食LEP降低了DSS诱导的疾病活动指数（DAI），结肠缩短和结肠组织损伤。LEP治疗通过调节紧密连接蛋白和粘液层保护蛋白的表达来恢复肠屏障的完整性。此外，LEP通过调节PPARγ/NF-κB和IL-6 / STAT3途径并抑制炎症细胞浸润来抑制促炎细胞因子的产生。此外，LEP还抑制了含有3（NLRP3）炎性小体激活的（NOD）样受体家族吡啶结构域，DSS诱导的内质网（ER）应力和氧化/亚硝化应力。这些结果为LEP作为保护小鼠免受DSS诱导的IBD的潜在天然药物提供了科学依据。