Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum


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Abstract

Graphical abstractHighlightsOverpressure blast injury (OBI) induces oxidative stress and inflammation in lung and brain.Repeated OBI causes edema and disrupts blood brain barrier while single injury has no significant effect.There is a positive correlation between blast injury induced brain edema and lung edema.Immunoreactivity of gliosis markers like Iba-1 and GFAP increased in the cortex after OBI. Moreover NF-κB and NGF proteins also increased.Tromboplastin activity rises in the brain tissue by repeated injury and this indicates that it is prone to bleeding after OBI.Serum leptin levels are significantly elevated after OBI.Background & aim:Overpressure blast-wave induced brain injury (OBI) and its long-term neurological outcome pose significant concerns for military personnel. Our aim is to investigate the mechanism of injury due to OBI.Methods:Rats were divided into 3 groups: (1) Control, (2) OBI (exposed 30 psi peak pressure, 2–2.5 ms), (3) Repeated OBI (r-OBI) (three exposures over one-week period). Lung and brain (cortex and cerebellum) tissues were collected at 24 h post injury.Results:The neurological examination score was worse in OBI and r-OBI (4.2 ± 0.6 and 3.7 ± 0.5, respectively) versus controls (0.7 ± 0.2). A significant positive correlation between lung and brain edema was found. Malondialdehyde (index for lipid peroxidation), significantly increased in OBI and r-OBI groups in cortex (p < 0.05) and cerebellum (p < 0.01–0.001). The glutathione (endogenous antioxidant) level decreased in cortex (p < 0.01) and cerebellum (p < 0.05) of r-OBI group when compared with the controls. Myeloperoxidase activity indicating neutrophil infiltration, was significantly (p < 0.01–0.05) elevated in r-OBI. Additionally, tissue thromboplastin activity, a coagulation marker, was elevated, indicating a tendency to bleed. NGF and NF-κB proteins along with Iba-1 and GFAP immunoreactivity significantly augmented in the frontal cortex demonstrating microglial activation. Serum biomarkers of injury, NSE, TNF-alpha and leptin, were also elevated.Conclusion:OBI triggers both inflammation and oxidative injury in the brain. This data in conjunction with our previous observations suggests that OBI triggers a cascade of events beginning with impaired cerebral vascular function leading to ischemia and chronic neurological consequences.

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