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dc.contributor.authorSharma A.
dc.contributor.authorMuresanu D.F.
dc.contributor.authorLafuente J.V.
dc.contributor.authorSjöquist P.-O.
dc.contributor.authorPatnaik R.
dc.contributor.authorTian Z.R.
dc.contributor.authorOzkizilcik A.
dc.contributor.authorSharma H.S.
dc.date.accessioned2020-09-02T22:28:13Z
dc.date.available2020-09-02T22:28:13Z
dc.date.issued2018
dc.identifier10.1007/s12035-017-0740-y
dc.identifier.citation55, 1, 276-285
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6244
dc.descriptionThe possibility that traumatic brain injury (TBI) occurring in a cold environment exacerbates brain pathology and oxidative stress was examined in our rat model. TBI was inflicted by making a longitudinal incision into the right parietal cerebral cortex (2 mm deep and 4 mm long) in coldacclimatized rats (5 °C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in coldexposed rats exhibited pronounced increase in brain lucigenin (LCG), luminol (LUM), and malondialdehyde (MDA) and marked pronounced decrease in glutathione (GTH) as compared to identical TBI at room temperature. The magnitude and intensity of BBB breakdown to radioiodine and Evans blue albumin, edema formation, and neuronal injuries were also exacerbated in cold-exposed rats after injury as compared to room temperature. Nanowired delivery of H-290/51 (50 mg/kg) 6 and 8 h after injury in cold-exposed group significantly thwarted brain pathology and oxidative stress whereas normal delivery of H-290/51 was neuroprotective after TBI at room temperature only. These observations are the first to demonstrate that (i) cold aggravates the pathophysiology of TBI possibly due to an enhanced production of oxidative stress, (ii) and in such conditions, nanodelivery of antioxidant compound has superior neuroprotective effects, not reported earlier. © Springer Science+Business Media, LLC 2017.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectBlood-brain barrier
dc.subjectBrain edema
dc.subjectCold environment
dc.subjectGlutathione
dc.subjectH-290/51
dc.subjectLucigenin
dc.subjectLuminol
dc.subjectMalondialdehyde
dc.subjectNanodelivery
dc.subjectNeuronal damage
dc.subjectOxidative stress
dc.subjectTraumatic brain injury (TBI)
dc.subjectantioxidant
dc.subjectglutathione
dc.subjectH 290 51
dc.subjecth 290 51
dc.subjectlucigenin
dc.subjectluminol
dc.subjectmalonaldehyde
dc.subjectnanowire
dc.subjecttitanium dioxide
dc.subjectunclassified drug
dc.subjectantioxidant
dc.subjectH290-51
dc.subjectindole derivative
dc.subjectnanowire
dc.subjectneuroprotective agent
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectblood brain barrier
dc.subjectbrain region
dc.subjectcold acclimatization
dc.subjectcontrolled study
dc.subjectdisease exacerbation
dc.subjectdose response
dc.subjectdrug delivery system
dc.subjectdrug effect
dc.subjectedema
dc.subjectenzyme activity
dc.subjectenzyme blood level
dc.subjectmale
dc.subjectneuropathology
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectparietal lobe
dc.subjectpathophysiology
dc.subjectrat
dc.subjectroom temperature
dc.subjecttraumatic brain injury
dc.subjectanimal
dc.subjectbrain
dc.subjectcold
dc.subjectmetabolism
dc.subjectoxidative stress
dc.subjectpathology
dc.subjectphysiology
dc.subjectSprague Dawley rat
dc.subjecttraumatic brain injury
dc.subjecttreatment outcome
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectBrain
dc.subjectBrain Injuries, Traumatic
dc.subjectCold Temperature
dc.subjectIndoles
dc.subjectMale
dc.subjectNanowires
dc.subjectNeuroprotective Agents
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectTreatment Outcome
dc.titleCold environment exacerbates brain pathology and oxidative stress following traumatic brain injuries: Potential therapeutic effects of nanowired antioxidant compound H-290/51
dc.typeArticle


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