Effects of hyperoxia exposure on the expression of Nrf2 and heme oxygenase-1 in lung tissues of premature rats.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease with long-term sequelae including neurodevelopmental delay. Although the precise mechanism of BPD is not well defined, oxidative stress is thought to be involved in the pathogenesis process of BPD. Nrf2 (Nuclear factor erythroid 2-related factor 2)-Keap1 (Kelch-like ECH associated protein 1)-ARE (Antioxidant Reaction Elements) signaling pathway is one of the main protective mechanisms of BPD, which can induce cytoprotective gene expression, such as heme oxygenase-1 (HO-1), nicotinamide quinone oxidoreductase 1 (NQO1) and so on. We exposed premature rats to hyperoxia and identified lung developmental retardation in preterm rats, with similar pathological changes as BPD. The expression of Nrf2 and HO-1 in premature rats was significantly higher after hyperoxia exposure. To explore the changes of Nrf2 and HO-1 in premature rats and enhance their beneficial functions may provide new treatment strategies for infants at risk of BPD.