Abstract
Recent studies have demonstrated that peroxisome proliferator-activated receptor-α (PPAR-α) agonists can protect the brain against excessive oxidative stress and inflammation in traumatic brain injury (TBI) and stroke through endogenous PPAR-α. However, it has not been investigated whether, and to what degree, cerebral expression of PPAR-α changes after TBI, especially in the human brain. In this study, 12 contused brain samples were obtained from 11 patients undergoing surgery for TBI 6–98 h after trauma. PPAR-α binding activity was measured by electrophoretic mobility shift assay, and temporal and cellular expression of PPAR-α by immunohistochemistry. The results showed that a persistent upregulation of PPAR-α binding activity and protein expression occurred in injured cortex after TBI, which peaked 24–72 h post-injury. Expression of PPAR-α was mainly located in glial and vascular endothelial cells with a little expression in the neurons. It is concluded that TBI could greatly upregulate the binding activity and protein expression of PPAR-α in injured human brain, which might be important in brain pathophysiology after TBI.