Objective To identify the differentially expressed genes of allergic rhinitis (AR) disease progression, explore the regulatory mechanism of its competing endogenous RNA (ceRNA) network, and screen potential therapeutic targets.Methods The GEO database was searched with download of AR's microarray chip GSE46171. Using R language and other software, the differential long non-coding RNA (lncRNA) and messenger RNA (mRNA) were analyzed. The microRNA (miRNA) that interacts with the differential lncRNA and the mRNAs it regulates were predicted through the public database, and then intersected with the differential mRNAs to obtain the lncRNA-miRNA-mRNA relationship to construct a ceRNA network. The STRING database and cytoscape software were used to screen key genes, and the DAVID database was used to analyze the gene functions and related pathways of key genes, and mine key ceRNA networks.Results ①Compared with normal nasal mucosa tissue, 35 lncRNAs and 2071 mRNAs were differentially expressed in nasal mucosa tissue of AR patients. ②Five key genes were screened out, including CREB1, PPARG, ETS1, IRF4, and JAK2. ③The enriched functions of key genes include biological processes such as myeloid differentiation and positive regulation of DNA binding involve signaling pathways such as Longevity, AMPK, and IL-17. ④ Six miRNAs (miR-27a-3p, miR-125a-5p, miR-135a-5p, miR-125b-5p, miR-17-5p, miR-20b-5p) may play key roles in the development of AR.Conclusion Through the analysis of the ceRNA network mediated by lncRNA related to AR, potential therapeutic targets and signal pathways are identified, which can further clarify its pathogenesis and provide a reference for subsequent experimental research.