Dexmedetomidine reduces oxidative stress and provides neuroprotection in a model of traumatic brain injury via the PGC-1α signaling pathway

Abstract

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-1α) expression. These findings imply that DEX protects neurons following TBI, possibly by activating the PGC-1α pathway. The data will help clarify the mechanisms responsible for the anti-apoptosis effect of DEX with possible involvement of the PGC-1α pathway.