MiR-216a-5p protects 16HBE cells from HO-induced oxidative stress through targeting HMGB1/NF-kB pathway.

Asthma is a complex, chronic inflammatory disorder of the bronchial tree, and can affect patients of all ages including children. High mobility group box 1 (HMGB1) has been proved as a therapeutic target in children with asthma, and was predicted to be the target gene of microRNA-216a-5p (miR-216a-5p). The present study aimed to investigate the function of miR-216a-5p in asthma by creating a human bronchial epithelial cell (16HBE) injury model using H₂O₂. A significantly elevation of HMGB1 protein expression and a reduction of miR-216a-5p expression were observed in children with asthma as well as in H₂O₂ stimulated 16HBE cells. Dual luciferase reporter assays confirmed the target reaction between HMGB1 and miR-216a-5p. MiR-216a-5p repressed HMGB1 protein expression in H₂O₂ induced 16HBE cells. Moreover, miR-216a-5p inhibited H₂O₂ induced cell injury by elevating cell proliferation and decreasing cell apoptosis in 16HBE cells. Furthermore, miR-216a-5p repressed NF-kB pathway activation in H₂O₂ induced 16HBE cells. In conclusion, these results suggested that miR-216a-5p functions as a negative regulator of H₂O₂ induced 16HBE cell injury through targeting HMGB1/NF-kB pathway, provided a potential therapeutic target for asthma.