Liu Xuemei, Chen Hong, Chen Xiaobo, Wu Peng, Zhang Jianhua
Department of Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China.
Department of Rehabilitation, The First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China.
Crit Rev Immunol. 2023;43(4):1-10. doi: 10.1615/CritRevImmunol.2023049479.
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.
本研究旨在运用网络药理学和分子对接技术，探究青藤碱治疗变应性鼻炎（AR）的潜在靶点及分子机制。从公共数据库获取青藤碱和AR的相关靶点，并在基因表达综合数据库中鉴定出AR的差异表达基因（DEG）。通过使用VennDiagram，我们通过交叉疾病靶点、药物靶点和DEG，确定了22个青藤碱抗AR的潜在靶点。功能分析表明，青藤碱可能通过其抗炎和免疫抑制作用发挥作用，其作用途径可能包括丝裂原活化蛋白激酶（MAPK）、缺氧诱导因子-1（HIF-1）和Janus激酶-信号转导子和转录激活子（JAK-STAT）途径。此外，使用极限点中心性（EPC）、最大团中心性（MCC）和最小邻居中心性（MNC）算法确定枢纽靶点，并通过整合前10个枢纽基因和22个潜在靶点，选择了6个枢纽靶点（信号转导子和转录激活子3（STAT3）、表皮生长因子受体（EGFR）、核因子κB亚基1（NFKB1）、缺氧诱导因子1α（HIF1A）、前列腺素内过氧化物合酶2（PTGS2）和Janus激酶1（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对与炎症和免疫相关的关键靶点和途径的调节。
