文章摘要
温扬敏*.基于网络药理学研究兖州卷柏对酒精肝损伤小鼠的保护作用[J].安徽医药,待发表.
基于网络药理学研究兖州卷柏对酒精肝损伤小鼠的保护作用
投稿时间:2022-12-19  录用日期:2023-01-18
DOI:
中文关键词: 兖州卷柏  网络药理学  酒精性肝病  黄酮类化合物  IL-17信号通路
英文关键词: 
基金项目:
作者单位邮编
温扬敏** 泉州医学高等专科学校 362000
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中文摘要:
      目的:利用网络药理学和动物实验研究兖州卷柏治疗酒精性肝病(alcoholic liver disease,ALD)的分子机制。方法:通过查阅文献和TCMSP数据库预测兖州卷柏有效成分及作用靶点,并通过靶点富集分析和分子对接预测兖州卷柏治疗ALD的作用机制。构建急性酒精性肝病小鼠模型,验证网络药理学预测结果。结果:网络靶点分析结果显示,从兖州卷柏中共筛选出治疗ALD的有效成分20个, 其中黄酮类化合物是治疗ALD的关键化合物。从兖州卷柏治疗ALD的65个靶点中筛选出6个核心靶点,核心靶点中除VEGFA外,均富集在SIL-17信号通路。分子对接结果显示,黄酮类关键化合物与核心靶点均具有较好的结合活性。动物实验结果显示,兖州卷柏总黄酮能显著降低ALD小鼠的AST和ALT活性(P < 0.05),改善酒精引起的肝损伤,抑制SIL-17信号通路关键基因mRNA表达。结论:黄酮类化合物是兖州卷柏治疗ALD的主要成分,可通过多靶点、多途径实现治疗ALD 的作用,其治疗机制可能与抑制IL-17信号通路有关。
英文摘要:
      Objective: The mechanism of Selaginella involven in the treatment of alcoholic liver disease (ALD) was explored on network pharmacology and animal experiment. Methods: The active compounds and relative targets of S. involven were predicted through literature review and TCMSP databases, and the mechanism of S. involven against ALD was analyzed by targets enrichment analysis and molecular docking. The network predictions were validated by establishing acute alcoholic liver injury mice model. Results: Based on the prediction results, 20 chemical compounds in the treatment of ALD were identified from S. involven, and flavonoids compounds were the main compounds in the treatment of ALD. 6 core targets screened from 65 ALD-related targets of S. involven, and the core targets were enriched in IL-17 signaling pathway except VEGFA. Molecular docking indicated that the main flavonoids compounds from S. involven showed good binding properties with the core targets. The results of animal experiments showed that acute alcoholic liver injury mice treated with total flavones of S.involventis significantly reduced the level of AST and ALT (P﹤0.05), alleviated pathological changes of liver tissues, and significantly inhibited the mRNA expression of core genes enrichment in IL-17 signaling pathway. Conclusion: Flavonoid compounds were the main active compounds of S.involventis in the treatment of ALD through multiple targets and multiple pathways, and its mechanisms maybe involved in inhibiting the IL-17 signaling pathway.
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