目的 基于整合文献挖掘和网络药理学探究黄葵胶囊治疗糖尿病肾病（DN）的作用机制。方法 通过中国学术期刊全文数据库（CNKI）、万方数据库和Web of Science文献检索平台获取黄蜀葵花化学成分，并借助PubChem数据库与ChemBioDraw软件下载化合物结构；借助Swiss Target Prediction和Stitch数据库预测化学成分相应靶点，并于CTD、DrugBank、GeneCards和TTD数据库中获得的DN靶点取交集，得到“成分-疾病”直接共有靶点；利用GeneMANIA获取间接靶点并借助Cytoscape软件构建蛋白质互作网络图；通过基因本体论和京都基因与基因组百科全书数据库（KEGG）对潜在相关靶点进行基因功能富集分析和通路富集分析，并构建黄蜀葵花治疗DN的“成分-直接靶点-间接靶点-通路”网络图。结果 经文献检索得到黄葵胶囊化学成分50个，数据库预测其治疗糖尿病肾病相关靶点182个，KEGG通路富集分析得到187个相关通路，其中6个关键通路可以通过参与调节多个生物过程改善DN疾病的发展。结论 通过文献挖掘与网络药理学初步揭示了黄葵胶囊参与调节机体糖脂代谢、氧化应激、炎症反应、血流动力学紊乱和自噬等生物过程改善DN疾病的发展。

Objective To study the mechanism of Huangkui capsule in the treatment of diabetic nephropathy (DN) based on literature mining and network pharmacology. Methods The constituents of A. manihot were obtained by CNKI、Wanfang database and Web of Science, and the PubChem database and the ChemBioDraw software were used to download the structures of the compounds. Then, the corresponding targets of chemical constituents were predicted in Swiss Target Prediction and Stitch database, and intersected with the DN targets predicted in CTD, DrugBank, GeneCards and TTD databases to obtain the direct targets of "component-disease". The indirect targets were obtained through GeneMANIA, and the protein interaction network map was constructed with the help of Cytoscape software. Finally, Gene ontology and KEGG database were to conduct the Gene function enrichment analysis and pathway enrichment analysis of potential related targets, and the "component-direct target-indirect targetpathway" network diagram of A. manihot in the treatment of DN was constructed. Results Totally 50 chemical constituents of A. manihot were obtained, 182 targets related to the treatment of DN were predicted and 187 pathways were obtained by KEGG pathway analysis, of which 6 key pathways can regulate multiple biological processes to improve the development of DN. Conclusions Through literature mining and network pharmacology, this study reveals that Huangkui Capsule can participate in regulating biological processes such as glucose and lipid metabolism, oxidative stress, inflammation, hemodynamic disorders and autophagy to improve the development of DN disease, which provides a basis for further study of related mechanisms.

R285.5