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

Abstract

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.

Cellular messenger molecules mediating addictive drug-induced cognitive impairment: cannabinoids, ketamine, methamphetamine, and cocaine

“…Cocaine-induced cognitive impairment is also associated with neuroinflammation and oxidative stress. Neuroinflammation causes cognitive aging and increases the generation of reactive oxygen species (ROS), thus inducing oxidative stress [56,57]. Notably, oxidative stress is considered an underlying causative factor of neurodegenerative diseases [58].…”

“…NF-κB, c-Fos, and FosB are required for the transcription of inflammatory cytokines, such as ILs, and induce an inflammatory response [59,60]. During inflammatory reactions, NF-κB and FosB are positively correlated, whereas superoxide dismutase (SOD) and glutathione peroxidase (GPx) elicit opposite outcomes [57]. Cocaine-dependent female subjects showed reduced executive functions and elevated plasma IL-6 levels [61].…”

Mechanism of Phosgene-Induced Acute Lung Injury and Treatment Strategy

“…Subsequently, a large number of inflammatory mediators and free radicals are released, causing oxidative stress and promoting alveolar and blood vessel damage, which eventually lead to the formation of noncardiogenic edema. Inflammation and oxidative stress are important mechanisms of sublethal phosgene damage, which is consistent with ALI caused by other factors such as bacteria [108], virus [109], smoke inhalation [110], and ex-plosion [111]. Therefore, anti-inflammatory or antioxidant drugs may have a therapeutic effect on ALI including P-ALI.…”

Identification of overlay differentially expressed genes in both rats and goats with blast lung injury through comparative transcriptomics

“… 9 The detailed method of BLI model was referenced from previously published papers by our research team. 10 , 11 …”