基于生物信息学及分子对接技术探究杜仲总黄酮治疗多囊卵巢综合征的作用机制

Exploring the Mechanism of Action of Total Flavonoids from Eucommia ulmoides in the Treatment of Polycystic Ovary Syndrome Based on Bioinformatics and Molecular Docking Technology

摘要: 研究旨在通过生物信息学与分子对接技术，探究杜仲总黄酮(TFE)治疗多囊卵巢综合征(PCOS)的潜在作用机制。研究人员首先从GEO数据库获取PCOS相关的转录组数据集(GSE277906)，筛选出差异表达基因(DEGs)。其次，对DEGs进行GO功能注释和KEGG通路富集分析，并构建蛋白质–蛋白质相互作用(PPI)网络。基于PPI网络分析，筛选出关键靶基因PECAM1、CD5和KLRB1。最后，采用分子对接技术验证了杜仲总黄酮(TFE)与这三个关键靶蛋白的结合能力。研究结果显示，TFE可能通过调控与免疫炎症(如白细胞黏附与迁移)和代谢(如胰岛素抵抗、类固醇激素生物合成)相关的信号通路，作用于PECAM1、CD5、KLRB1等核心靶点，从而发挥治疗PCOS的多靶点协同效应。

Abstract: This study aims to investigate the potential mechanism of total flavonoids from Eucommia ulmoides (TFE) in the treatment of polycystic ovary syndrome (PCOS) using bioinformatics and molecular docking approaches. Researchers first retrieved PCOS-related transcriptomic datasets (GSE277906) from the GEO database and screened differentially expressed genes (DEGs). Subsequently, GO functional annotation and KEGG pathway enrichment analyses were performed on the DEGs, followed by the construction of a protein-protein interaction (PPI) network. Based on PPI network analysis, three core target genes—PECAM1, CD5, and KLRB1—were identified. Finally, molecular docking was employed to validate the binding affinity between TFE and these three key target proteins. The results suggest that TFE may exert multi-target synergistic effects in treating PCOS by modulating signaling pathways associated with immune inflammation (e.g., leukocyte adhesion and migration) and metabolism (e.g., insulin resistance and steroid hormone biosynthesis), primarily acting on core targets including PECAM1, CD5, and KLRB1.