Literature DB >> 31836968

The Changes of Brain Edema and Neurological Outcome, and the Probable Mechanisms in Diffuse Traumatic Brain Injury Induced in Rats with the History of Exercise.

Nasrin Soltani1, Zahra Soltani2, Mohammad Khaksari3, Ghasem Ebrahimi4, Mojdeh Hajmohammmadi1, Maryam Iranpour5.   

Abstract

Since no definitive treatment has been suggested for diffuse traumatic brain injury (TBI), and also as the effect of exercise has been proven to be beneficial in neurodegenerative diseases, the effect of endurance exercise on the complications of TBI along with its possible neuroprotective mechanism was investigated in this study. Our objective was to find out whether previous endurance exercise influences brain edema and neurological outcome in TBI. We also assessed the probable mechanism of endurance exercise effect in TBI. Rats were randomly assigned into four groups of sham, TBI, exercise + sham and exercise + TBI. Endurance exercise was carried out before TBI. Brain edema was assessed by calculating the percentage of brain water content 24 h after the surgery. Neurological outcome was evaluated by obtaining veterinary coma scale (VCS) at - 1, 1, 4 and 24 h after the surgery. Interleukin-1β (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), protein carbonyl and histopathological changes were evaluated 24 h after the surgery. Previous exercise prevented the increase in brain water content, MDA level, histopathological edema and apoptosis following TBI. The reduction in VCS in exercise + TBI group was lower than that of TBI group. In addition, a decrease in the level of serum IL-1β and the content of brain protein carbonyl was reported in exercise + TBI group in comparison with the TBI group. We suggest that the previous endurance exercise prevents brain edema and improves neurological outcome following diffuse TBI, probably by reducing apoptosis, inflammation and oxidative stress.

Entities:  

Keywords:  Apoptosis; Brain injury; Inflammation; Interleukin-1β; Malondialdehyde; Oxidative stress; Protein carbonyl

Mesh:

Substances:

Year:  2019        PMID: 31836968     DOI: 10.1007/s10571-019-00753-w

Source DB:  PubMed          Journal:  Cell Mol Neurobiol        ISSN: 0272-4340            Impact factor:   5.046


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