Objective：This study aims to investigate the effects of early postnatal hyperoxia exposure on ovalbumin（OVA）- induced bronchial asthma mice. Methods：Thirty-two female BALB/c pups were randomly assigned to four groups：Room Air-PBS group，Hyperoxia-PBS group，Room Air-OVA group，and Hyperoxia-OVA group，with 8 mice in each group. Mice in Hyperoxia-PBS group and Hyperoxia-OVA group were exposed to hyperoxia（FiO2 ≥ 95%）for 7 days，meanwhile mice in Room Air-PBS group and Room Air-OVA group were raised in room air（FiO2 = 21%）. After 7 days，the Hyperoxia-PBS group and Hyperoxia-OVA group were removed from hyperoxia and raised in the same environment with the Room Air-PBS group and the Room Air-OVA group. Mice in Room Air-OVA group and Hyperoxia-OVA group were given intraperitoneal injection of sensitization suspension［OVA 1 mg /mL + Al（OH）3］from d65. All the animals were sacrificed for bronchoalveolar lavage，and the lavage fluid was collected for leukocyte count. The levels of IL-5，IL-12，IL-13 in bronchoalveolar lavage fluid（BALF）and IgE in serum were measured by ELISA. The lung tissue of mice in each group was analysis by histological staining for pathological changes. Results：The level of serum IgE in Hyperoxia-OVA group was significantly higher than that in Air -OVA group（P < 0.05）；The counts of eosinophils，lymphocytes and monocytes in BALF were increased（P < 0.05），the levels of IL-5 and IL-13 were increased，but the level of IL-12 was decreased（P < 0.05）；Inflammatory cells infiltration，bronchial stenosis，and airway wall thickening were observed，airway wall thickness area ratio was increased（P < 0.05），structural remodeling was obvious；radial alveolar count（RAC）was increased significantly（P < 0.05）in the Hyperoxia-OVA group. Conclusion：Early postnatal hyperoxia exposure can aggravate the airway inflammation of ovalbumin induced asthma mice，airway structure remodeling is obvious，but the lung injury is reduced.