Open Access

Intermittent hypoxia simulating obstructive sleep apnea causes pulmonary inflammation and activates the Nrf2/HO‑1 pathway

  • Authors:
    • Yeying Wang
    • Yanling Chai
    • Xiaojie He
    • Li Ai
    • Xia Sun
    • Yiling Huang
    • Yongxia Li
  • View Affiliations

  • Published online on: August 18, 2017     https://doi.org/10.3892/etm.2017.4971
  • Pages: 3463-3470
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Obstructive sleep apnea (OSA) is a disorder with high morbidity in adults. OSA damages multiple organs and tissues, including the cardiovascular and cerebrovascular systems, the metabolism system, the lungs, liver and heart. OSA‑induced damage is earliest and greatest to the pulmonary tissue. The present study established a rat OSA model of differing severity by inducing intermittent hypoxia with different concentrations of O2 and it was determined that OSA caused a severe oxidative stress response and pulmonary inflammation in a dose‑dependent manner. OSA increased serum levels of C‑reactive protein and 8‑isoprostane and elevated the expression of malondialdehyde, tumor necrosis factor α, interleukin (IL)‑1β and IL‑6 in the pulmonary tissue. Furthermore, the expression of two important antioxidants, superoxide dismutase and glutathione, was downregulated following intermittent hypoxia. By contrast, levels of cylooxygenase 2 and inducible nitric oxide synthase, which are crucial in the antioxidative response, increased. In addition, OSA activates the nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase (OH)‑1 antioxidative signaling pathway. Finally, all increases and decreases in levels of inflammatory and antioxidative substances were dependent on oxygen concentrations. Therefore, the present study demonstrated that OSA, simulated by intermittent hypoxia, caused an oxidative stress response and pulmonary inflammation, and activated the canonical antioxidative Nrf2/HO‑1 signaling pathway in a dose‑dependent manner. These results may facilitate the development of clinical therapies to treat pulmonary diseases caused by OSA.

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October-2017
Volume 14 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Wang Y, Chai Y, He X, Ai L, Sun X, Huang Y and Li Y: Intermittent hypoxia simulating obstructive sleep apnea causes pulmonary inflammation and activates the Nrf2/HO‑1 pathway. Exp Ther Med 14: 3463-3470, 2017.
APA
Wang, Y., Chai, Y., He, X., Ai, L., Sun, X., Huang, Y., & Li, Y. (2017). Intermittent hypoxia simulating obstructive sleep apnea causes pulmonary inflammation and activates the Nrf2/HO‑1 pathway. Experimental and Therapeutic Medicine, 14, 3463-3470. https://doi.org/10.3892/etm.2017.4971
MLA
Wang, Y., Chai, Y., He, X., Ai, L., Sun, X., Huang, Y., Li, Y."Intermittent hypoxia simulating obstructive sleep apnea causes pulmonary inflammation and activates the Nrf2/HO‑1 pathway". Experimental and Therapeutic Medicine 14.4 (2017): 3463-3470.
Chicago
Wang, Y., Chai, Y., He, X., Ai, L., Sun, X., Huang, Y., Li, Y."Intermittent hypoxia simulating obstructive sleep apnea causes pulmonary inflammation and activates the Nrf2/HO‑1 pathway". Experimental and Therapeutic Medicine 14, no. 4 (2017): 3463-3470. https://doi.org/10.3892/etm.2017.4971