
@article{ref1,
title="Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum",
journal="Behavioural brain research",
year="2018",
author="Toklu, Hale Z. and Yang, Zhihui and Oktay, Şehkar and Sakarya, Yasemin and Kirichenko, Nataliya and Matheny, Michael K. and Muller-Delp, Judy and Strang, Kevin and Scarpace, Philip J. and Wang, Kevin K. W. and Tümer, Nihal",
volume="340",
number="",
pages="14-22",
abstract="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. <br><br>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. <br><br>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. <br><br>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.<br><br>Copyright © 2017. Published by Elsevier B.V.<p /> <p>Language: en</p>",
language="en",
issn="0166-4328",
doi="10.1016/j.bbr.2017.04.025",
url="http://dx.doi.org/10.1016/j.bbr.2017.04.025"
}