Network pharmacology analysis and experimental verification reveal the mechanism of the traditional Chinese medicine YU-Pingfeng San alleviating allergic rhinitis inflammatory responses

Zhen Liu; Qi Sun; Xinyue Liu; Zheying Song; Fei Song; Congxian Lu; Yu Zhang; Xicheng Song; Yujuan Yang; Yumei Li

doi:10.3389/fpls.2022.934130

Network pharmacology analysis and experimental verification reveal the mechanism of the traditional Chinese medicine YU-Pingfeng San alleviating allergic rhinitis inflammatory responses

Front Plant Sci. 2022 Aug 9:13:934130. doi: 10.3389/fpls.2022.934130. eCollection 2022.

Authors

Zhen Liu^{1

2}, Qi Sun^{1

2}, Xinyue Liu^{1

2}, Zheying Song^{1

2

3}, Fei Song^{1

2

4}, Congxian Lu^{1

2}, Yu Zhang^{1

2}, Xicheng Song^{1

2}, Yujuan Yang^{1

2}, Yumei Li^{1

2}

Affiliations

¹ Department of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China.
² Shandong Provincial Clinical Research Center for Otorhinolaryngologic Diseases, Yantai, China.
³ Clinical Medicine College, Weifang Medical University, Weifang, China.
⁴ Second Clinical Medicine College, Binzhou Medical University, Yantai, China.

Abstract

YU-Pingfeng San (YPFS) can regulate inflammatory response to alleviate the symptoms of nasal congestion and runny rose in allergic rhinitis (AR). However, the mechanism of action remains unclear. In this study, 30 active ingredients of three effective herbs included in YPFS and 140 AR/YPFS-related genes were identified by database analysis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that the targets were mainly enriched in immune inflammatory-related biological processes and pathways. Finally, three hub gene targeting epidermal growth factor receptor (EGFR), mitogen-activated protein kinase 1 (MAPK1), and protein kinase B1 (AKT1) related to YPFS and AR were identified by network pharmacology analysis. YPFS treatment decreased the expression of EGFR, MAPK1, and AKT1 in ovalbumin (OVA)-induced AR mice and impaired the production of inflammatory factors interleukin (IL)-4, IL-5, and IL-13, thus alleviating immunoglobulin E (IgE) production and the symptoms of scratching nose in AR. Through molecular docking analysis, we found that the active ingredients decursin, anomalin, and wogonin of YPFS could bind to EGFR, MAPK1, and AKT1 proteins. Moreover, decursin treatment impaired the expression of IL-4 and IL-5 in human PBMCs. These results suggested that YPFS could alleviate the AR inflammatory responses by targeting EGFR, MAPK1, and AKT1, showing the mechanism of action of YPFS in AR treatment.

Keywords: YPFS; allergic rhinitis; decursin; hub genes; network pharmacology analysis.