HDAC3‐mediated lncRNA ZFAS1 inhibited IL‐13‐induced secretion of proinflammatory cytokines in nasal epithelial cells by regulating the miR‐7‐5p/SIRT1 pathway

Allergic rhinitis (AR) is a disease that is difficult to cure and accompanies the patient's life. Proinflammatory cytokines (GM‑CSF and eotaxin) and MUC5AC are key mediators promoting AR progression. Herein, the function of lncRNA ZFAS1 in AR was investigated. Nasal epithelial cells (NECs) were subjected to 50 ng/mL IL‐13 for 24 h to construct an AR cell model. The mRNA and protein expressions were assessed using qRT‐PCR and western blot. The levels of GM‑CSF, eotaxin, IL‐1β, IL‐6, TNF‐α and MUC5AC in cell supernatant were examined by ELISA. The binding relationships between HDAC3, ZFAS1, miR‐7‐5p and SIRT1 were analysed using dual luciferase reporter or ChIP assays. Herein, our results displayed that ZFAS1 and SIRT1 were lowly expressed in AR, while miR‐7‐5p and HDAC3 were highly expressed. Functional experiments displayed that ZFAS1 overexpression suppressed IL‐13‐induced proinflammatory cytokines and mucin production in NECs. The highly expressed HDAC3 in AR inhibited ZFAS1 expression by binding with ZFAS1 promoter. In addition, our experiments revealed that ZFAS1 targeted miR‐7‐5p, and miR‐7‐5p targeted SIRT1. As expected, miR‐7‐5p overexpression or SIRT1 silencing abrogated ZFAS1 upregulation's repression on IL‐13‐induced proinflammatory cytokines and MUC5AC secretory levels in NECs. ZFAS1 suppressed proinflammatory cytokines, inflammatory cytokines, and MUC5AC secretory levels in AR by regulating the miR‐7‐5p/SIRT1 axis. Thus, our work suggested that ZFAS1 might serve as a novel target for AR treatment and prevention.