| 张盼盼,陈莹莹,何玉霞.黄芪多糖调控Wnt/β-catenin通路对结核杆菌感染小鼠的保护作用.[J].中南医学科学杂志.,2025,(1):32-35, 117. |
| 黄芪多糖调控Wnt/β-catenin通路对结核杆菌感染小鼠的保护作用 |
| Protective effects of astragalus polysaccharide on mice infected with Mycobacterium tuberculosis by Wnt/β-catenin pathway |
| 投稿时间：2024-04-08 修订日期：2024-12-05 |
| DOI：10.15972/j.cnki.43-1509/r.2025.01.007 |
| 中文关键词: 黄芪多糖 Wnt/β-catenin通路 结核杆菌 炎症因子 小鼠 [ |
| 英文关键词:astragalus polysaccharide Wnt/β-catenin pathway Mycobacterium tuberculosis mechanism of action mice |
| 基金项目:沧州市科技计划项目(162302097) |
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| 中文摘要: |
| 目的研究黄芪多糖调控Wnt/β-catenin通路对结核杆菌感染小鼠模型的保护作用及可能机制。 方法将C57BL/6小鼠随机均分为对照组、模型组、黄芪多糖组及黄芪多糖+Wnt/β-catenin通路抑制剂组(黄芪多糖+iCRT组)。小鼠除对照组外均成功建立结核杆菌感染模型。比较各组炎症因子、免疫指标、肺质量指数、脾质量指数、肺组织病理学形态改变、肺组织结核菌荷菌量以及通路相关因子Wnt、β-catenin、Cyclin D1蛋白表达水平。 结果模型组、黄芪多糖组、黄芪多糖+iCRT组白细胞介素(IL)-10、免疫球蛋白(Ig)G、IgM、CD4＋/CD8＋水平以及Wnt、β-catenin、Cyclin D1蛋白表达较对照组降低,IL-6、γ干扰素(IFN-γ)、肺质量指数、脾质量指数、荷菌量较对照组升高(P＜0.05)。黄芪多糖组IL-10、IgG、IgM、CD4＋/CD8＋水平以及Wnt、β-catenin、Cyclin D1蛋白表达较模型组升高,IL-6、IFN-γ、肺质量指数、脾质量指数、荷菌量较模型组降低(P＜0.05)。模型组肺组织结构受损严重,出现明显炎症细胞浸润及肺泡腔狭窄,可见结核结节形成。黄芪多糖组肺组织病变有明显改善。与黄芪多糖组比较,黄芪多糖+iCRT组上述趋势均得到明显逆转(P＜0.05)。 结论黄芪多糖可能通过激活Wnt/β-catenin通路抑制结核杆菌感染小鼠肺组织荷菌量和炎症反应,提高免疫功能,从而发挥肺保护作用。 |
| 英文摘要: |
| AimTo study the protective effects of astragalus polysaccharide on mice infected with Mycobacterium tuberculosis by Wnt/β-catenin pathway. MethodsC57BL/6 mice were randomly divided into control group, model group, astragalus polysaccharide group and astragalus polysaccharide + Wnt/β-catenin pathway inhibitor group (astragalus polysaccharide + iCRT group). The Mycobacterium tuberculosis infection model was successfully established in all mice except the control group. The inflammatory factors, immune indexes, lung mass index, spleen mass index, lung tissue pathological morphological changes, lung tissue Mycobacterium tuberculosis load and pathway-related factors Wnt, β-catenin, Cyclin D1 protein expression levels were compared among the groups. ResultsThe interleukin(IL)-10, immunoglobulin (Ig) G, IgM, CD4＋/CD8＋ levels and Wnt, β-catenin, and Cyclin D1 protein expressions in the model group, astragalus polysaccharide group, and astragalus polysaccharide + iCRT group were lower than those in the control group, while IL-6, interferon-γ (IFN-γ), lung mass index, spleen mass index, and bacterial load were higher than those in the control group (P＜0.05). The levels of IL-10, IgG, IgM, CD4＋/CD8＋, and the expression of Wnt, β-catenin, and Cyclin D1 proteins in the APS group were higher than those in the model group, while the levels of IL-6, IFN-γ, lung mass index, spleen mass index, and bacterial load were lower than those in the model group (P＜0.05). The lung tissue structure in the model group was severely damaged, with obvious inflammatory cell infiltration, alveolar stenosis, and formation of tuberculosis nodules. The lung tissue lesions in the APS group were significantly improved. Compared with the APS group, the above trends in the APS+iCRT group were significantly reversed (P＜0.05). ConclusionAPS may inhibit the bacterial load and inflammatory response of the lung tissue of mice infected with Mycobacterium tuberculosis by activating the Wnt/β-catenin pathway, improve immune function, and thus play a protective role in lung. |
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