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Cold Environment Exacerbates Brain Pathology and Oxidative Stress Following Traumatic Brain Injuries: Potential Therapeutic Effects of Nanowired Antioxidant Compound H-290/51
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. Uppsala Univ, Int Expt CNS Injury & Repair, Univ Hosp, Frodingsgatan 12,Bldg 28, SE-75421 Uppsala, Sweden.;Univ Basque Country UPV EHU, Dept Neurosci, LaNCE, Leioa, Bizkaia, Spain..
RoNeuro Inst Neurol Res & Diagnost, 37 Mircea Eliade St, Cluj Napoca 400364, Romania.;Univ Med & Pharm, Dept Clin Neurosci, Cluj Napoca, Romania..
Univ Basque Country UPV EHU, Dept Neurosci, LaNCE, Leioa, Bizkaia, Spain.;BioCruces Hlth Res Inst, Nanoneurosurg Grp, Baracaldo 48903, Bizkaia, Spain.;Univ Autonoma Chile, Fac Hlth Sci, Santiago, Chile..
Karolinska Univ Hosp, Karolinska Inst, Div Cardiol, Dept Med, Stockholm, Sweden..
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 276-285Article in journal (Refereed) Published
Abstract [en]

The 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 cold-acclimatized rats (5 degrees C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in cold-exposed 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.

Place, publisher, year, edition, pages
Humana Press, 2018. Vol. 55, no 1, p. 276-285
Keywords [en]
Traumatic brain injury (TBI), Oxidative stress, Luminol, Lucigenin, Malondialdehyde, Glutathione, H-290/51, Nanodelivery, Blood-brain barrier, Brain edema, Neuronal damage, Cold environment
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:uu:diva-346900DOI: 10.1007/s12035-017-0740-yISI: 000424702600028PubMedID: 28856566OAI: oai:DiVA.org:uu-346900DiVA, id: diva2:1195136
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved

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Sharma, ArunaSharma, Hari S.

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