Lab for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering, Key Lab for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, NPU-UAB Joint Laboratory for Bone Metabolism, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, China.
Research Center for Toxicological and Biological Effects, Institute for Hygiene of Ordnance Industry, Xi'an 710065, China.
Acta Biochim Biophys Sin (Shanghai). 2021 Mar 2;53(3):283-293. doi: 10.1093/abbs/gmaa179.
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 changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.
爆震性肺损伤（BLI）是爆炸冲击波致伤导致死亡的主要原因，但 BLI 的发病机制尚不清楚。为了明确 BLI 的时相变化特点，采用燃料空气炸药建立大鼠爆震伤模型，通过苏木精-伊红（HE）染色和病理评分评估模型，同时检测肺组织炎症反应和氧化应激变化。结果显示，伤后 2 h、24 h、3 d、7 d 大鼠肺组织病理评分分别为 9.75±2.96、13.00±1.85、8.50±1.51、4.00±1.41，与对照组（1.13±0.64）比较差异均有统计学意义（P<0.05）。伤后 2 h 和 24 h 大鼠呼吸频率和呼吸暂停时间明显增加，呼气峰流量、吸气时间和分钟呼气量逐渐减少，呈时间依赖性变化。伤后 2 h 和 24 h 时，白细胞介素（IL）-6、IL-8、FosB 和核转录因子（NF）-κB 等炎症因子表达明显增加，于 24 h 达高峰，3 d 后逐渐下降，2 周后基本恢复正常。伤后 24 h 时，大鼠总抗氧化能力、总超氧化物歧化酶和谷胱甘肽过氧化物酶水平明显降低，丙二醛水平于 24 h 时达高峰。这些结果表明，冲击波诱导的炎症和氧化应激反应呈时间依赖性显著变化，可能是 BLI 治疗的重要因素和新的治疗靶点。
