miR-124-3p relieves allergic rhinitis by inhibiting dipeptidyl peptidase-4.

MicroRNA-124-3p (miR-124-3p) and dipeptidyl peptidase-4 (DPP4) are closely related to the development of inflammation. Allergic rhinitis (AR) models in mice and HNEpC cells were established. AR progression was assessed assessing by the frequency of nasal rubbing and sneezing, hematoxylin and eosin (HE), and TUNEL staining. Tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor (GM-CSF), eotaxin, and MUC5AC were assessed by enzyme-linked immunosorbent assay and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Apoptosis in HNEpC cells was assessed using flow cytometry. DPP4, activated-caspase-3, and pro-caspase-3 protein expression were evaluated by western blotting. In addition, we clarified the influence of miR-124-3p-targeted DPP4 on AR inflammation and cell injury. MiR-124-3p was downregulated in AR nasal mucosa tissue. Upregulation of miR-124-3p reduced the frequency of nasal rubbing and sneezing, pathological changes, eosinophil number, and apoptosis of nasal mucosa, TNF-α and IL-6 protein and mRNA levels in serum and HNEpC cells, and MUC5AC, eotaxin, and GM-CSF levels in HNEpC cells. Downregulation of miR-124-3p has the opposite effect. Therefore, the miR-124-3p /DPP4 axis may be an attractive target for AR therapy.