NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

作者：Hong Wang, Wenjuan Zhang, J. Liu, Junhong Gao, Le Fang, Zhiyong Liu, Bao-Qing Xia, Xiaolin Fan, Cunzhi Li, Qing Lü, Airong Qian · 发表于：Acta Biochimica et Biophysica Sinica · 年份：2021 · DOI：10.1093/abbs/gmaa179 · 被引用次数：18 · 研究领域：Burn Injury Management and Outcomes、Effects of Radiation Exposure、Disaster Response and Management

Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats' lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P<0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves change...