Journal
NEUROPEPTIDES
Volume 72, Issue -, Pages 58-64Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.npep.2018.10.004
Keywords
Dexmedetomidine; Traumatic brain injury; PGC-1 alpha; Oxidative stress
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The protective effects of dexmedetomidine (DEX) mediated by reductions of oxidative stress, mitochondrial damage and disintegration have been demonstrated in many injury models. However, whether DEX has a beneficial effect on traumatic brain injury (TBI) remains unknown. In this study, the neuroprotective effect of DEX and its potential mechanism were assessed in a model of TBI. DEX treatment relieved encephala edema and neuron cell apoptosis and increased behavioral function. These protective effects were accompanied by upregulation of peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1 alpha) expression. These findings imply that DEX protects neurons following TBI, possibly by activating the PGC-1 alpha pathway. The data will help clarify the mechanisms responsible for the anti-apoptosis effect of DEX with possible involvement of the PGC-1 alpha pathway.
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