Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine.
Mona ShehadehPalzur EilamLiat ApelJean Francois SoustielPublished in: International journal of molecular sciences (2019)
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.
Keyphrases
- cerebral ischemia
- traumatic brain injury
- peripheral nerve
- subarachnoid hemorrhage
- oxidative stress
- cell death
- spinal cord injury
- blood brain barrier
- severe traumatic brain injury
- resting state
- white matter
- public health
- heat shock protein
- computed tomography
- amino acid
- high glucose
- functional connectivity
- binding protein
- drug induced
- young adults
- multiple sclerosis
- cell proliferation
- pet imaging
- replacement therapy
- endoplasmic reticulum