【Abstract】 Objective To investigate whether the expression level of microRNA-22-3p (miR-22-3p) and the neurokinin receptor 1 (NK1R) in juvenile asthmatic airway remodeling rats are affected by the expression level of miR-22-3p. Methods Forty eight Wistar rats were divided into control group, model group, model+mimic group, model+mimic NC group, model+inhibitor group and model+inhibitor NC group. The control group was injected with normal saline and inhaled air; the model group was established with ovalbumin (OVA) atomization inhalation method; the model+mimic group, model+mimic NC group, model+inhibitor group and model+inhibitor NC group were injected with 1 mL of mimic, mimic NC, inhibitor and inhibitor NC by tail vein within 1 hour before each challenge. The changes of airway remodeling were observed by H & E staining and Mir-22-3p was detected by RTqPCR. Luciferase gene reporter assay was used to verify that Mir-22-3p targeted NK1R in rat airway smooth muscle cells (RASMCs). The expression of NK1R was detected by Western blot and immunohistochemistry. Results Compared with the control group, significant airway remodeling was observed in the model group, and the level of Mir-22-3p in the airway tissue was decreased (P＜0.05). In RASMCs, the direct binding of 3 ′-UTR and Mir-22-3p of NK1R resulted in the decrease of luciferase activity (P＜0.05). Compared with the control group, the expression of NK1R mRNA and protein in the model group was significantly upregulated (P＜0.01). Compared with model+mimic NC group, the expression of Mir-22-3p in model+mimic group was upregulated, while the expression of NK1R was down regulated (P＜0.05). Compared with model+inhibitor NC group, the level of Mir-22-3p was down regulated in model+inhibitor NC group, while NK1R level was upregulated (P＜0.05). Conclusion The expression of NK1R in airway of asthmatic rats was increased. Mir-22-3p could directly target and inhibit the expression of NK1R in airway remodeling of asthmatic rats, and down regulate Mir-22-3p to relieve the inhibition of NK1R, thus increasing the level of NK1R.