Up-Regulated miR-20b-5p Mitigates Cell Inflammation and Apoptosis in Allergic Rhinitis via STAT3.

Abstract

Allergic rhinitis (AR) is a highly prevalent, chronic hypersensitivity reaction of the nasal mucosa. The exact function of miR-20b-5p in AR is currently unknown. The purpose of this study was to investigate the relationship between miR-20b-5p and illness risk, as well as its function in AR. One hundred and seventy-six patients provided blood samples. Human nasal epithelial cells (NEPCs) stimulated with 50 ng/mL interleukin-13 (IL-13) created the in vitro research model of AR. A receiver operator characteristic (ROC) curve was used to illustrate the miR-20b-5p clinical predictive value. Cell transfection was used to regulate gene expression. By using qRT-PCR, the expression levels of signal transducer and activator of transcription 3 (STAT3) and miR-20b-5p were examined. The CCK-8 kit was used to measure cell viability. Using a flow cytometer, cell apoptosis was found. Enzyme-linked immunosorbent assay (ELISA) was used to investigate the serum IgE and the inflammatory evaluation, which included MUC5AC, eotaxin, GM-CSF. The dual luciferase reporter system was employed to confirm the targeting link between miR-20b-5p and STAT3. The relative miR-20b-5p level was diminished in AR patients, in addition to human NEPCs induced with IL-13. Up-regulation of miR-20b-5p inverted decreased cell viability and elevated cell apoptosis. Moreover, the content of inflammatory cytokines MUC5AC, eotaxin, and GM-CSF was strengthened after IL-13 treatment, and highly expressed miR-20b-5p restrained the levels of inflammation dramatically. ROC curves with high sensitivity and specificity suggested miR-20b-5p as a potential biomarker for illness prediction. STAT3 was a potential downstream target of miR-20b-5p. miR-20b-5p serves as a candidate biomarker for AR. Enhanced miR-20b-5p can inhibit nasal epithelial cell inflammation and apoptosis.