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Citation
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Toklu HZ, Yang Z, Oktay Ş, Sakarya Y, Kirichenko N, Matheny MK, Muller-Delp J, Strang K, Scarpace PJ, Wang KKW, Tümer N. Behav. Brain Res. 2018; 340: 14-22. |
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Affiliation
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Geriatric Research Education & Clinical Center, Malcolm Randall Veterans Affairs Medical Center, FL, USA; University of Florida Departments of Pharmacology & Therapeutics, College of Medicine Department of Biomedical Sciences, FL, USA. Electronic address: ntumer@ufl.edu. |
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Abstract
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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 30psi peak pressure, 2-2.5ms), 3) Repeated OBI (r-OBI) (three exposures over one-week period). Lung and brain (cortex and cerebellum) tissues were collected at 24h 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-ĸB 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.
Copyright © 2017. Published by Elsevier B.V.
Language: en |