Oxidative stress and expression of inflammatory factors in lung tissue of acute mountain sickness rats

The aim of the present study was to investigate the changes in lung histomorphology and oxidative stress, as well as the expression of interleukin (IL)‑17C and other inflammatory factors during acute mountain sickness (AMS) in male Sprague‑Dawley rats and to explore the underlying mechanism. Rats were randomly divided into a control group (0 h) and three hypoxia stress groups, exposed to low‑pressure oxygen storage at a simulated altitude of 6,000 m for 24, 48 and 72 h, respectively. Morphological changes in lung tissue were observed by hematoxylin and eosin staining under light microscopy and transmission electron microscopy. The expression of inflammatory factors IL‑17C, nuclear factor‑κB (NF‑κB), IL‑1β, IL‑6 and tumor necrosis factor‑α (TNF‑α) in lung tissue was assessed by RNA sequencing and verified by reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting (WB). Superoxide dismutase (SOD) and glutathione peroxidase (GSH‑Px) enzyme activity and malondialdehyde (MDA) expression were also measured. Experimental groups were compared to the control group following 24, 48 and 72 h of hypoxic stress. Lung tissue suffered from different degrees of injury, and the damage was the most severe after 48 h of hypoxic stress. RNA sequencing data from the lung tissue of rats from each group suggested that the expression of IL‑17C, NF‑κB, IL‑1β, IL‑6, and TNF‑α increased significantly after hypoxic stress. RT‑qPCR and WB demonstrated that the expression of IL‑17C and NF‑κB increased significantly after hypoxia lasting 48 and 72 h. IL‑1β expression increased significantly after hypoxia stress lasting 24 and 48 h, and the expressions of TNF‑α and IL‑6 increased significantly after hypoxia stress lasting 24, 48 and 72 h (P