Conclusion
Our findings suggest that tempol effectively relieves OSA-induced lung injury.
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-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.
Results
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.