This study aimed to explore the ameliorative effects and potential mechanisms of Huangshan Umbilicaria esculenta polysaccharide (UEP) in dextran sulfate sodium-induced acute ulcerative colitis (UC) and UC secondary liver injury (SLI). Results showed that UEP could ameliorate both colon and liver pathologic injuries, upregulate mouse intestinal tight junction proteins (TJs) and MUC2 expression, and reduce LPS exposure, thereby attenuating the effects of the gut–liver axis. Importantly, UEP significantly downregulated the secretion levels of TNF-α, IL-1β, and IL-6 through inhibition of the NF-κB pathway and activated the Nrf2 signaling pathway to increase the expression levels of SOD and GSH-Px. In vitro, UEP inhibited the LPS-induced phosphorylation of NF-κB P65 and promoted nuclear translocation of Nrf2 in RAW264.7 cells. These results revealed that UEP ameliorated UC and SLI through NF-κB and Nrf2-mediated inflammation and oxidative stress. The study first investigated the anticolitis effect of UEP, suggesting its potential for the treatment of colitis and colitis-associated liver disease.

中文翻译：

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石耳多糖对DSS所致小鼠结肠炎及继发性肝损伤的保护作用及机制研究

本研究旨在探讨黄山石耳多糖（UEP）对右旋糖酐硫酸钠诱导的急性溃疡性结肠炎（UC）和UC继发性肝损伤（SLI）的改善作用及其潜在机制。结果表明，UEP 可以改善结肠和肝脏病理损伤，上调小鼠肠道紧密连接蛋白 (TJ) 和 MUC2 表达，并减少 LPS 暴露，从而减弱肠-肝轴的影响。重要的是，UEP通过抑制NF-κB通路显着下调TNF-α、IL-1β和IL-6的分泌水平，并激活Nrf2信号通路以增加SOD和GSH-Px的表达水平。在体外，UEP 抑制 LPS 诱导的 NF-κB P65 磷酸化并促进 RAW264.7 细胞中 Nrf2 的核转位。这些结果表明，UEP 通过 NF-κB 和 Nrf2 介导的炎症和氧化应激改善 UC 和 SLI。该研究首先调查了 UEP 的抗结肠炎作用，表明其治疗结肠炎和结肠炎相关肝病的潜力。