Back to Search Start Over

Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat

Authors :
Mohd Salman
Suhel Parvez
Heena Tabassum
Pooja Kaushik
Source :
Cellular and Molecular Neurobiology. 41:765-781
Publication Year :
2020
Publisher :
Springer Science and Business Media LLC, 2020.

Abstract

Excessive mitochondrial fission has been implicated in the etiology of neuronal cell death in traumatic brain injury (TBI). In the present study, we examined the efficacy of melatonin (Mel) as a neuroprotective agent against TBI-induced oxidative damage and mitochondrial dysfunction. We assessed the impact of Mel post-treatment (10 mg/kg b.wt., i.p.) at different time intervals in TBI-subjected Wistar rats. We found that the Mel treatment significantly attenuated brain edema, oxidative damage, mitochondrial fission, and promoted mitochondrial fusion. Additionally, Mel-treated rats showed restoration of mitochondrial membrane potential and oxidative phosphorylation with a concomitant reduction in cytochrome-c release. Further, Mel treatment significantly inhibited the translocation of Bax and Drp1 proteins to mitochondria in TBI-subjected rats. The restorative role of Mel treatment in TBI rats was supported by the mitochondrial ultra-structural analysis, which showed activation of mitochondrial fusion mechanism. Mel enhanced mitochondrial biogenesis by upregulation of PGC-1α protein. Our results demonstrated the remedial role of Mel in ameliorating mitochondrial dysfunctions that are modulated in TBI-subjected rats and provided support for mitochondrial-mediated neuroprotection as a putative therapeutic agent in the brain trauma.

Details

ISSN :
15736830 and 02724340
Volume :
41
Database :
OpenAIRE
Journal :
Cellular and Molecular Neurobiology
Accession number :
edsair.doi.dedup.....d3db39454db22a06ffaae4efb6a7e5de
Full Text :
https://doi.org/10.1007/s10571-020-00884-5