Abstract
Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague-Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.
Original language | English |
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Article number | 2639 |
Journal | International Journal of Molecular Sciences |
Volume | 20 |
Issue number | 11 |
DOIs | |
State | Published - 29 May 2019 |
Bibliographical note
Publisher Copyright:© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Funding
Funding: This study was funded by a grant of the Galilee Clinical Bio Research Center.
Funders | Funder number |
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Galilee Clinical Bio Research Center |
Keywords
- Etifoxine
- Mitochondria
- Mitochondrial permeability transition pore
- Translocator protein
- Traumatic brain injury