Intratracheal Surfactant Administration Attenuates Hyperoxia-Induced Lung Injury and Fibrosis in Neonatal Rats

Abstract Background: Hyperoxia decreases surfactant production and suggests exogenous surfactant may be a potential treatment for hyperoxia-induced lung injury. This study aimed to investigate the effects of an animal-derived surfactant on hyperoxia-induced lung injury and fibrosis in newborn rats. Methods: Sprague Dawley rat pups were randomly reared either in room air (RA) or hyperoxic conditions (85% O 2 ) from postnatal days 1–14. On postnatal day 4, the rats received an intratracheal injection of either 20 μL of normal saline (vehicle) or 20 μL of surfactant (Survanta). Our study included four study groups: RA + vehicle, RA + surfactant, 85% O 2 + vehicle, and 85% O 2 + surfactant. Body weights were recorded at birth and on postnatal days 4 and 14. On postnatal day 14, the lungs were dissected for histology, Western blotting, and cytokine measurements. Results: The hyperoxia-reared rats exhibited significantly higher lung injury scores, tumor necrosis factor-α (TNF-α) expression, transforming growth factor-β1 (TGF-β1) expression, and collagen deposition compared with the RA-reared rats. The surfactant alleviated hyperoxia-induced lung injury, inflammation, and fibrosis, as evidenced by the lower lung injury score, TNF-α expression, TGF-β1 expression, and collagen deposition in the lungs. Conclusion: The intratracheal administration of the surfactant ameliorated hyperoxia-induced lung injury and fibrosis and downregulated TNF-α and TGF-β1 expression, most likely by inhibiting lung inflammation and collagen deposition.