Author/Authors :
-، - نويسنده Department of quality management, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province, China Yu, Shouli , -، - نويسنده Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China Shi, Min , -، - نويسنده Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China Liu, Qinghui , -، - نويسنده Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China Liu, Changting , -، - نويسنده Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China Guo, Jun , -، - نويسنده Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China Yu, Senyang , -، - نويسنده Respiratory Department, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province, China Jiang, Tingshu
Abstract :
Objective(s):Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI).
Materials and Methods: In this study, we investigated the time course changes of oxidative stress and inflammation in lung tissues of rats exposed to >95% oxygen for 12-60 hr.
Results: We found that at 12 hr after hyperoxia challenge, the activities of superoxide dismutase and glutathione peroxidase were significantly reduced with remarkably increased lipid peroxidation. At 12 hr, NF-κB p65 expression was also upregulated, but Iκ-Bα expression showed a remarkable decline. Significant production of inflammatory mediators, e.g, interleukin-1β, occurred 24 hr after hyperoxia exposure. In addition, the expression of intracellular adhesion molecule 1 expression and the activity of myeloperoxidase were significantly increased at 24 hr with a peak at 48 hr.
Conclusion: Our data support that hyperoxia-induced oxidative damage and NF-κB pathway activation implicate in the early phase of HALI pathogenesis.
