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

Le résumé fourni par la source

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.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.