Fig. 6

MiR-493-5p agomiR attenuates allergic airway inflammation and airway hyperreactivity. BALB/c mice were divided into 4 groups (n = 8 for each group), control, asthma, miR-493-5p agomiR and agomiR NC. MiR-493-5p agomiR or agomiR NC was dropped into the nasal cavities of the asthma model mice before the models were stimulated by OVA. A, B miR-493-5p agomiR treatment significantly reduced the proportion of Th9 cells, and the protein production of FOXO1, IL-9 and IRF4 in OVA-induced asthma mice were significantly reduced. C The protein production of FOXO1, IRF4 and IL-9 in lung tissue was detected by western blot. D Groups. E–G The protein production of FOXO1, IRF4 and IL-9 in lung tissue was analyzed by Western blot and quantified using ImageJ software. H–J The mRNA expression of IL-9, IRF4 and FOXO1 was detected by RT-qPCR. K The HE staining results showed a large number of inflammatory cells infiltrated around the bronchi and blood vessels, inflammatory cells and exudates increased, epithelial cells edema and lumen stenosis were observed in OVA-induced asthma mice. Compared with the OVA-induced asthma mice following with agomiR NC treatment, the inflammatory reaction dramatically attenuated in miR-493-5p agomiR treatment mice. L The airway hyperreactivity, miR-493-5p agomiR treatment significantly inhibited the airway hyper-responsiveness in OVA-induced asthma mice (**P < 0.01 compared to agomiR NC group). ^**P < 0.01 compared to A group, ^##P < 0.01 compared to B group