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

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dc.contributor.authorOKTAY, NİHAL ŞEHKAR
dc.contributor.authorsToklu, Hale Z.; Yang, Zhihui; Oktay, Sehkar; Sakarya, Yasemin; Kirichenko, Nataliya; Matheny, Michael K.; Muller-Delp, Judy; Strang, Kevin; Scarpace, Philip J.; Wang, Kevin K. W.; Tumer, Nihal
dc.date.accessioned2022-03-12T22:27:32Z
dc.date.available2022-03-12T22:27:32Z
dc.date.issued2018
dc.description.abstractBackground & 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-kappa B 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.
dc.identifier.doi10.1016/j.bbr.2017.04.025
dc.identifier.eissn1872-7549
dc.identifier.issn0166-4328
dc.identifier.pubmed28419850
dc.identifier.urihttps://hdl.handle.net/11424/235214
dc.identifier.wosWOS:000424173400002
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofBEHAVIOURAL BRAIN RESEARCH
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectOverpressure blast injury
dc.subjectBrain
dc.subjectTrauma
dc.subjectLung
dc.subjectEdema
dc.subjectNGF
dc.subjectNF kappa B
dc.subjectGFAP
dc.subjectIba1
dc.subjectNSE
dc.subjectTRAUMATIC BRAIN-INJURY
dc.subjectSUBARACHNOID HEMORRHAGE
dc.subjectBARRIER PERMEABILITY
dc.subjectBLOOD
dc.subjectMODEL
dc.subjectINFLAMMATION
dc.subjectDAMAGE
dc.subjectEXPRESSION
dc.subjectBIOMARKERS
dc.subjectSEVERITY
dc.titleOverpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum
dc.typearticle
dspace.entity.typePublication
local.avesis.ida259aa57-d0ea-45d8-ae75-ba935f0a5df0
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages9
local.journal.quartileQ2
oaire.citation.endPage22
oaire.citation.startPage14
oaire.citation.titleBEHAVIOURAL BRAIN RESEARCH
oaire.citation.volume340
relation.isAuthorOfPublicationeaf67f2d-ce76-4abc-afe1-ec62645dfe87
relation.isAuthorOfPublication.latestForDiscoveryeaf67f2d-ce76-4abc-afe1-ec62645dfe87

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