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    薛永举, 杨丽, 柯希权, 朱玉, 王猛. 姜黄素联合5-氨基水杨酸介导Notch信号通路治疗溃疡性结肠炎大鼠的分子机制研究[J]. 蚌埠医科大学学报, 2023, 48(9): 1185-1192. DOI: 10.13898/j.cnki.issn.1000-2200.2023.09.002
    引用本文: 薛永举, 杨丽, 柯希权, 朱玉, 王猛. 姜黄素联合5-氨基水杨酸介导Notch信号通路治疗溃疡性结肠炎大鼠的分子机制研究[J]. 蚌埠医科大学学报, 2023, 48(9): 1185-1192. DOI: 10.13898/j.cnki.issn.1000-2200.2023.09.002
    shu
    XUE Yong-ju, YANG Li, KE Xi-quan, ZHU Yu, WANG Meng. Molecular mechanism of curcumin combined with 5-aminosalicylic acid-mediated Notch signaling pathway in the treatment of ulcerative colitis rats[J]. Journal of Bengbu Medical University, 2023, 48(9): 1185-1192. DOI: 10.13898/j.cnki.issn.1000-2200.2023.09.002
    Citation: XUE Yong-ju, YANG Li, KE Xi-quan, ZHU Yu, WANG Meng. Molecular mechanism of curcumin combined with 5-aminosalicylic acid-mediated Notch signaling pathway in the treatment of ulcerative colitis rats[J]. Journal of Bengbu Medical University, 2023, 48(9): 1185-1192. DOI: 10.13898/j.cnki.issn.1000-2200.2023.09.002
    shu

    姜黄素联合5-氨基水杨酸介导Notch信号通路治疗溃疡性结肠炎大鼠的分子机制研究

    Molecular mechanism of curcumin combined with 5-aminosalicylic acid-mediated Notch signaling pathway in the treatment of ulcerative colitis rats

      摘要
    • 摘要:
      目的探讨Notch信号通路在溃疡性结肠炎(UC)大鼠发病中的可能作用及姜黄素通过该信号通路治疗UC大鼠的分子机制。
      方法按照将2 mL/kg三硝基苯磺酸注入结肠的方法制备大鼠UC模型。实验设对照组、UC模型组、5-氨基水杨酸(5-ASA)组、姜黄素组、姜黄素+5-氨基水杨酸(5-ASA)组，每组各6只。后3组每天灌胃1次，连续10 d。同时每日观察大鼠一般情况，并且记录其每天的疾病活动指数评分，在连续10 d给予不同处理方式后，取大鼠结肠组织进行结肠黏膜损伤指数评分、HE染色分析，观察统计大鼠结肠黏膜损伤情况，用免疫组织化学法、Western blotting法检测大鼠结肠黏膜内Notch1、jaggled1、Hes1蛋白表达，RT-PCR检测大鼠结肠黏膜内Notch1、jaggled1、Hes1 mRNA表达。
      结果HE染色结果表明模型组与对照组相比，出现了显著性病理损伤，5-ASA和姜黄素治疗组病理损伤有所减缓(P<0.01)；姜黄素+5-ASA联合治疗组病理损伤减缓效果最佳(P<0.01)。免疫组织化学结果、Western blotting结果及RT-PCR结果显示与对照组比较，模型组Notch1、jaggledl、Hes1 mRNA表达水平均上升(P<0.01)；与模型组相比，5-ASA和姜黄素治疗组大鼠黏膜组织中Notch1、jaggledl、Hes1表达下降(P<0.01)，而姜黄素+5-ASA联合治疗组Notch1、jaggledl、Hes1下降趋势最明显(P<0.01)。
      结论姜黄素对UC有一定的治疗作用，可能与参与介导Notch信号通路有关。

       

      Abstract:
      ObjectiveTo explore the possible role of Notch signaling pathway in the pathogenesis of ulcerative colitis (UC) in rats and the molecular mechanism of curcumin treating UC in rats through Notch signaling pathway.
      MethodsA rat UC model was prepared by injecting 2 mL/kg of trinitrobenzenesulfonic acid into the colon.There were five groups including control group, UC model group, 5-aminosalicylic acid (5-ASA) group, curcumin group, and curcumin+5-ASA group, with 6 rats in each group.The last three groups were applied intragastrically once a day for 10 consecutive days.Meanwhile, the general condition of rats was observed daily, and the disease activity index was recorded.After 10 days of treatment, the colonic tissues of rats was taken to carry out the colonic mucosa damage?index score and HE staining for observing the colonic mucosal injury of rats; immunohistochemistry and Western blotting were used to detect the protein expression of Notch1, jaggled1, and Hes1 in rat colonic mucosa; RT-PCR was applied to analyze the mRNA expression of Notch1, jaggled1, and Hes1 in rat colonic mucosa.
      ResultsThe HE staining results showed that there appeared significant pathological damage in the model group compared to the control group, and the pathological damage in the 5-ASA group and curcumin group was alleviated (P<0.01); the alleviated pathological damage in the curcumin+5-ASA group was the most obvious (P<0.01).The results of immunohistochemistry, Western blotting, and RT-PCR showed that compared with the control group, the mRNA expression levels of Notch1, jaggledl, and Hes1 in the model group increased (P<0.01); compared with the model group, the expression of Notch1, jaggledl, and Hes1 in the mucosal tissue of rats in the 5-ASA group and curcumin group decreased (P<0.01), and the decrease level in Notch1, jaggledl, and Hes1 was most significant in the curcumin+5-ASA group (P<0.01).
      ConclusionsCurcumin has a certain therapeutic effect on UC, which may be related to its involvement in mediating the Notch signaling pathway.

       

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