基于网络药理学探讨芪榆三黄膏治疗肛肠术后创面愈合不良的作用机制

目的 基于网络药理学探讨芪榆三黄膏治疗肛肠术后创面愈合不良的作用机制。方法 采用中医药系统药理学数据库(TCMSP)对芪榆三黄膏的活性成分进行筛选，并利用Swiss Target Prediction数据库预测其活性成分的潜在靶点；使用 Genecards数据库、Disgenet数据库和OMIM数据库检索肛肠病术后创面愈合不良的相关靶点；通过STRING数据库构建药物与疾病交集靶点的蛋白互作网络(PPI)，获得芪榆三黄膏治疗肛肠病术后创面愈合不良的关键靶标；运用DAVID 数据库对关键靶标进行基因本体论(GO)功能与基因组百科全书(KEGG)信号通路富集分析，并搭建疾病-通路-靶点-成分-药物网络。结果 筛选得到芪榆三黄膏的药效成分91个、药物靶点154个、肛肠术后创面愈合不良靶点679个，最终得到药物-疾病关键靶点26个，富集分析后获得175 个 GO 功能项目和 68 条 KEGG 信号通路。结论 芪榆三黄膏的活性成分可经PI3K-Akt、IL-17、MAPK、AGE-RAGE等通路，作用于TNF、IL-2、AKT1、EGFR、GSK3B等靶点，来发挥抑制炎症反应、促进血管再生、调控细胞增殖和凋亡等作用。

Exploring the Mechanism of Qiyu Sanhuang Ointment in Treating Poor Wound Healing after Anorectal Surgery Based on Network Pharmacology

Objective To explore the mechanism of Qiyu Sanhuang Ointment in the treatment of poor wound healing after anorectal surgery based on network pharmacology. Methods The active components of Qiyu Sanhuang ointment were screened by Traditional Chinese Medicine Systems Pharmacology Database(TCMSP), and the potential targets of its active components were predicted by Swiss Target Prediction database. Genecards database, Disgenet database and OMIM database were used to search the related targets of poor wound healing after anorectal surgery. The protein interaction network (PPI) of drug and disease intersection targets was constructed by STRING database, and the key targets of Qiyu Sanhuang ointment in the treatment of poor wound healing after anorectal surgery were obtained. The DAVID database was used to perform gene ontology(GO) function and genome encyclopedia(KEGG) signal pathway enrichment analysis on key targets, and the disease-pathway-target-component-drug network was built. Results A total of 91 pharmacodynamic components, 154 drug targets and 679 targets of poor wound healing after anorectal surgery were screened out. Finally, 26 key targets of drug-disease were obtained. After enrichment analysis, 175 GO functional items and 68 KEGG signaling pathways were obtained. Conclusion The active components of Qiyu Sanhuang ointment can be regulated by PI3K-Akt, IL-17, MAPK, AGE-RAGE and other pathways act on TNF, IL-2, AKT1, EGFR, GSK3 B and other targets to inhibit inflammatory response, promote angiogenesis, regulate cell proliferation and apoptosis.