Yeying Wang - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Bing Hai - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Li Ai - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Yu Cao - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Ran Li - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Hui Li - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China
Yongxia Li - Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan ۶۵۰۱۰۱, People’s Republic of China

Objective(s): Obstructive sleep apnea (OSA) is confirmed to cause lesions in multiple organs, especially in the lung tissue. Tempol is an antioxidant that has been reported to restrain inflammation and oxidative stress, with its role in OSA-induced lung injury being unclear. This study aimed to investigate the beneficial effect of tempol on chronic intermittent hypoxia (IH)-induced lung injury.Materials and Methods: A rat model of OSA was established by IH. There were four groups: normal air (NA), IH, IH+tempol, NA+tempol. Inflammatory response was evaluated by TNF-α, IL-۱β, and IL-۶ levels. Oxidative stress was detected by MDA and GSH levels, and SOD activity. The protein levels were assessed by Western blot. DNA binding activity of NF-κB or Nrf۲ was determined by electrophoretic mobility shift assay.Results: According to the results, tempol administration alleviated pathological changes of the lung tissue, decreased leukocyte count and protein content (P<۰.۰۰۱) in bronchoalveolar lavage fluid (BALF). Inflammation response in lung tissue induced by IH was suppressed by tempol as evidenced by decreased levels of TNF-α, IL-۱β, and IL-۶ (P<۰.۰۰۱) and protein levels of COX-۲ and iNOS (P<۰.۰۰۱). Moreover, tempol inhibited oxidative stress in lung tissue by down-regulating the MDA level (P<۰.۰۰۱) and enhancing SOD activity (P<۰.۰۰۱) and the GSH level (P<۰.۰۵). In addition, tempol repressed inflammation response via inactivation of the NF-κB pathway. Furthermore, the results suggested that tempol repressed oxidative stress by activating the Nrf۲/HO-۱ pathway. Conclusion: Our findings suggest that tempol effectively relieves OSA-induced lung injury.

Inflammation response, Intermittent hypoxia, NF-κB, Nrf۲/HO-۱, Oxidative stress, Tempol