The effect of oxygenation level on cerebral post‐traumatic apoptotsis is modulated by the 18‐kDa translocator protein (also known as peripheral‐type benzodiazepine receptor) in a rat model of cortical contusion

Abstract

The present findings suggest that the protective effect of hyperoxia may be due to a negative regulation of the proapoptotic function of mitochondrial TSPO, including conservation of the mitochondrial membrane potential.