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    邓学杰, 王振. 新鱼腥草素钠通过抑制STAT3/NF-κB信号通路的激活改善小鼠炎症性肠病[J]. 徐州医科大学学报, 2021, 41(8): 570-574.
    引用本文: 邓学杰, 王振. 新鱼腥草素钠通过抑制STAT3/NF-κB信号通路的激活改善小鼠炎症性肠病[J]. 徐州医科大学学报, 2021, 41(8): 570-574.
    shu
    Sodium new houttuyfonate alleviated Inflammatory bowel disease in mice by inhibiting the STAT3/NF-kB pathway activation[J]. Journal of Xuzhou Medical University, 2021, 41(8): 570-574.
    Citation: Sodium new houttuyfonate alleviated Inflammatory bowel disease in mice by inhibiting the STAT3/NF-kB pathway activation[J]. Journal of Xuzhou Medical University, 2021, 41(8): 570-574.
    shu

    新鱼腥草素钠通过抑制STAT3/NF-κB信号通路的激活改善小鼠炎症性肠病

    Sodium new houttuyfonate alleviated Inflammatory bowel disease in mice by inhibiting the STAT3/NF-kB pathway activation

      摘要
    • 摘要: 目的 研究新鱼腥草素钠（SNH）对炎症性肠病（IBD）小鼠的治疗效果及对STAT3/NF-kB的调控作用。方法 将24只小鼠随机分为空白对照组（CON组）、IBD模型组（IBD组）、药物干预组（SNH组），按照3% DSS造模法对IBD及SNH组小鼠进行造模，SNH组予以药物灌胃，CON组和IBD组予以生理盐水灌胃，共持续2周。每日监测各组小鼠体重、粪便稠度和便血，并测定疾病活动指数（DAI），通过HE染色法观察各组小鼠结肠组织形态变化及结肠组织病理学评分变化，采用Western blot法检测各组小鼠结肠组织STAT3、NF-κB蛋白表达水平变化，ELISA方法检测小鼠血清中的炎症因子IL-6、TNF-α、IL-18的表达。结果 SNH能够明显提高IBD小鼠的体重（P＜0.05），缓解IBD小鼠的腹泻、便血和结肠组织损伤，降低疾病活动指数（P＜0.05）。Western blot结果显示，与CON相比，IBD组结肠组织STAT3、NF-κB蛋白表达水平明显升高（P均<0.01），与IBD组相比，SNH组结肠组织STAT3、NF-κB蛋白表达水平明显降低（P均<0.01）；ELISA法结果显示，IBD组血浆中炎症因子IL-6、TNF-α及IL-18明显升高（P均<0.001），予以SNH干预后，SNH组的IL-6、TNF-α及IL-18炎症因子比IBD组明显降低（P均<0.01）。结论 SNH具有改善 DSS所致小鼠肠道炎症的效果，其作用机制可能与通过抑制STAT3/NF-κB通路的激活进而降低IL-6、TNF-α及IL-18炎症因子的表达有关。

       

      Abstract: ob＜x＞jective To investigate the therapeutic effect of Sodium new houttuyfonate (SNH) on (Inflammatory bowel disease，IBD) and the regulation of STAT3/NF-kB/ pathway. Methods Twnety-four mice were randomized into blank control group, IBD group and SNH group. Mice in the IBD and SNH groups were given 3% DSS in drinking water to induce IBD. The mice in SNH group were given SNH by gavage (25mg/kg) for 2 weeks, and the mice in CON group and IBD group were administrated with saline. The body weight, fecal consistency and hematochezia of mice in diverse groups were monitored daily for the measurement of the disease activity index (DAI). HE staining was used to observe the histopathological changes. The levels of colon tissue STAT3 and NF-κB were measured by Western blot. The levels of IL-6, TNF-α and IL-18 in plasma were detected by ELISA. Results The results showed that SNH administration significantly increased the body weights (P＜0.05), ameliorated diarrhea, hematochezia and colonic tissue damage, as well as reduced disease activity index in IBD mice (P＜0.05). The result of WB showed that colonic tissue STAT3/NF-κB levels were notably increased in IBD group compared to CON group (P<0.01). Moreover, the levels of STAT3/NF-κB were lower in SNH group than that in IBD group (P<0.01). The levels of plasma IL-6,TNF-α and IL-18 in groups of IBD group were increased compared to CON group ( P<0.01). The levels of plasma IL-6, TNF-α and IL-18 were decreased in SNH group compared to IBD group ( P<0.01). Conclusion SNH may contribute to suppressing inflammation via down-regulating the ex＜x＞pression of STAT3, NF-κB in colonic tissue and reducing the levels of IL-6,TNF-α and IL-18 cytokines, thereby alleviating the progression of the IBD

       

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