Department of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, 230031, China.
School of Public Health and Health Management, Anhui Medical College, Hefei, 230601, China.
Comb Chem High Throughput Screen. 2023;26(12):2161-2169. doi: 10.2174/1386207326666230127151049.
Xinfeng capsule (XFC) is a well-known drug against rheumatoid arthritis (RA). However, the combination mechanisms of XFC on RA remain unclear.
The purpose of this study is to explore the mechanisms of XFC against RA in terms of compounds, targets, and signaling pathways via network pharmacology.
The bioactive compounds and potential targets of XFC were extracted from TCMSP and BATMAN-TCM database, and the putative RA-related targets were determined from the DisGeNET, PHGKB, PharmGKB, and CTD database. The approach of protein-protein interaction, gene ontology analysis, and kyoto encyclopedia of genes and genomes pathway enrichment analysis were constructed, respectively. In animal experiments, we evaluated the expression of core targets.
We found that XFC handled 30 active compounds and 131 common target genes. Among them, mairin, folic acid, cholesterol, and triptolide in XFC were selected as the central active compounds against RA. The mechanisms of XFC on RA which concerned critical targets were protein kinase B (AKT1) and tumor necrosis factor (TNF). In vivo, we found that the expression levels of AKT1 and TNF in the modeling group were significantly increased but reversed by XFC.
The combination mechanisms of XFC were elucidated in terms of components and targets and signaling pathways, which may be related to inhibiting the proliferation of synovial cells and inflammation.
新风胶囊（XFC）是一种治疗类风湿性关节炎（RA）的知名药物。然而，XFC 治疗 RA 的联合机制尚不清楚。
本研究旨在通过网络药理学探讨 XFC 治疗 RA 的化合物、靶点和信号通路机制。
从 TCMSP 和 BATMAN-TCM 数据库中提取 XFC 的生物活性化合物和潜在靶点，并从 DisGeNET、PHGKB、PharmGKB 和 CTD 数据库中确定潜在的 RA 相关靶点。分别构建蛋白质-蛋白质相互作用、基因本体分析和京都基因与基因组百科全书通路富集分析方法。在动物实验中，我们评估了核心靶点的表达。
我们发现 XFC 处理了 30 种活性化合物和 131 个共同靶基因。其中，XFC 中的马里因、叶酸、胆固醇和雷公藤红素被选为治疗 RA 的核心活性化合物。XFC 治疗 RA 的机制涉及关键靶点蛋白激酶 B（AKT1）和肿瘤坏死因子（TNF）。在体内，我们发现模型组中 AKT1 和 TNF 的表达水平显著增加，但 XFC 可使其逆转。
从成分、靶点和信号通路方面阐明了 XFC 的联合作用机制，可能与抑制滑膜细胞增殖和炎症有关。
