Citation

Sharma A, Muresanu DF, Lafuente JV, Sjöquist PO, Patnaik R, Ryan Tian Z, Ozkizilcik A, Sharma HS. Mol. Neurobiol. 2018; 55(1): 276-285.

Affiliation

LaNCE, Department Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Bizkaia, Spain. Sharma@surgsci.uu.se.

Copyright

(Copyright © 2018, Springer)

DOI

10.1007/s12035-017-0740-y

PMID

28856566

Abstract

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 °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.

Language: en

Keywords

Blood-brain barrier; Brain edema; Cold environment; Glutathione; H-290/51; Lucigenin; Luminol; Malondialdehyde; Nanodelivery; Neuronal damage; Oxidative stress; Traumatic brain injury (TBI)