The present study was designed to explore the impact of hyperoxia on lung injury and fibrosis via the angiotensin II (AngII)-p22phox‑reactive oxygen species (ROS) signaling pathway, apoptosis and 8‑oxoguanine‑DNA glycosylase 1 (OGG1) repair enzyme. Newborn Sprague‑Dawley rats were randomly divided in the newborn air group, newborn hyperoxia group and newborn intervention group, the latter of which was administered the chymotrypsin inhibitor, 2-(5-formylamino-6-oxo-2-phenyl-1, 6‑dihydropyrimidine‑1‑yl)‑N‑[4‑dioxo‑1‑phenyl‑7‑(2‑pyridyloxy)]​2‑heptyl‑acetamide (NK3201). A group of adult rats also received hyperoxic treatment. Histomorphological changes in lung tissues were dynamically observed. AngII, ROS, angiotensin type 1 receptor (AT1R) and p22phox messenger RNA (mRNA) levels, and OGG1 and peroxisome proliferator‑activated receptor‑γ (PPARγ) protein levels in the lung tissues were detected at various times after hyperoxia. Hyperoxia led to traumatic changes in the lungs of newborn rats that resulted in decreased viability, increased mortality, morphological changes and the apoptosis of alveolar type II epithelial cells (AT‑II), as well as increased expression levels of AngII, AT1R and p22phox, which would ultimately lead to secondary diseases. NK3201 significantly inhibited the hyperoxia‑induced increased expression of AngII, AT1R and p22phox and further promoted OGG1 and PPARγ protein expression, thus reducing the intrapulmonary ROS level, the apoptotic index and caspase‑3 levels. However, the adult hyperoxia group only exhibited tachypnea and reduced viability. This study suggested that the AngII‑p22phox‑ROS signaling pathway, PPARγ and OGG1 together contributed to the hyperoxia‑induced lung injury and that NK3201 was able to reverse the effects of hyperoxia.

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