Tempol relieves lung injury in a rat model of chronic intermittent hypoxia via suppression of inflammation and oxidative stress

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. 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-1β, and IL-6 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 Nrf2 was determined by electrophoretic mobility shift assay. According to the results, tempol administration alleviated pathological changes of the lung tissue, decreased leukocyte count and protein content (P<0.001) 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-1β, and IL-6 (P<0.001) and protein levels of COX-2 and iNOS (P<0.001). Moreover, tempol inhibited oxidative stress in lung tissue by down-regulating the MDA level (P<0.001) and enhancing SOD activity (P<0.001) and the GSH level (P<0.05). 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 Nrf2/HO-1 pathway. Our findings suggest that tempol effectively relieves OSA-induced lung injury