This study aimed to investigate the potential targets and molecular mechanism of sinomenine in treating allergic rhinitis (AR) using network pharmacology and molecular docking. Relevant targets of sinomenine and AR were obtained from public databases, and differentially expressed genes (DEGs) for AR were identified in the Gene Expression Omnibus database. Using VennDiagram, we identified 22 potential targets of sinomenine against AR by crossing disease targets, drug targets, and DEGs. Functional analysis revealed that sinomenine may act via its anti-inflammatory and immunosuppressive effects, and its action pathways may include the MAPK, HIF-1, and JAK-STAT pathways. Furthermore, hub targets were identified using EPC, MCC, and MNC algorithms, and six hub targets (STAT3, EGFR, NFKB1, HIF1A, PTGS2, and JAK1) were selected by integrating the top 10 hub genes and 22 potential targets. Molecular docking analysis indicated that STAT3, EGFR, PTGS2, and JAK1 may be key targets of sinomenine against AR. Overall, our results suggest that sinomenine has potential therapeutic effects against AR, and its mechanism of action may involve the regulation of key targets and pathways related to inflammation and immunity.

中文翻译：

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基于网络药理学和分子对接识别青藤碱治疗过敏性鼻炎的潜在靶点和机制

本研究旨在通过网络药理学和分子对接探讨青藤碱治疗过敏性鼻炎（AR）的潜在靶点和分子机制。从公共数据库中获取青藤碱和AR的相关靶点，并在Gene Expression Omnibus数据库中鉴定出AR的差异表达基因（DEG）。使用 VennDiagram，我们通过交叉疾病靶点、药物靶点和 DEG 确定了青藤碱对抗 AR 的 22 个潜在靶点。功能分析表明，青藤碱可能通过抗炎和免疫抑制作用发挥作用，其作用途径可能包括MAPK、HIF-1和JAK-STAT途径。此外，使用EPC、MCC和MNC算法识别枢纽靶标，并通过整合前10个枢纽基因和22个潜在靶标选择6个枢纽靶标（STAT3、EGFR、NFKB1、HIF1A、PTGS2和JAK1）。分子对接分析表明STAT3、EGFR、PTGS2和JAK1可能是青藤碱抗AR的关键靶点。总体而言，我们的结果表明青藤碱对AR具有潜在的治疗作用，其作用机制可能涉及调节炎症和免疫相关的关键靶点和通路。