Nrf2‑Keap1‑ARE‑NQO1 signaling attenuates hyperoxia‑induced lung cell injury by inhibiting apoptosis

Bronchopulmonary dysplasia (BPD) is one of the main causes chronic lung disease in premature infants. Acute injury following exposure to hyperoxia contributes development BPD preterm The nuclear factor‑erythroid 2‑related factor 2 (Nrf2) signaling pathway an endogenous antioxidant defense mechanism that involved pathogenesis numerous hyperoxia‑induced diseases. In present study, expression Nrf2, Kelch‑like ECH‑associated protein 1 (Keap1) and NAD(P)H quinone oxidoreductase enzyme (NQO1) was detected A549 cells exposed transfection with small interfering RNA (siRNA) using reverse transcription‑quantitative polymerase chain reaction western blotting, cellular apoptosis flow cytometry. results demonstrated increased significantly hyperoxia, Keap1 NQO1 levels were upregulated under hyperoxic conditions. Furthermore, Nrf2 siRNA, these genes downregulated compared respective values untransfected cells. These findings suggest Nrf2‑Keap1‑antioxidant response element‑NQO1 may play a protective role via inhibition apoptosis.