Previous physical exercise alters the hepatic profile of oxidative‐inflammatory status and limits the secondary brain damage induced by severe traumatic brain injury in rats

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12495-list-0001">An early inflammatory response and oxidative stress are implicated in the signal transduction that alters both hepatic redox status and mitochondrial function after traumatic brain injury (TBI).Peripheral oxidative/inflammatory responses contribute to neuronal dysfunction after TBIExercise training alters the profile of oxidative‐inflammatory status in liver and protects against acute hyperglycaemia and a cerebral inflammatory response after TBI.Approaches such as exercise training, which attenuates neuronal damage after TBI, may have therapeutic potential through modulation of responses by metabolic organs.The vulnerability of the body to oxidative/inflammatory in TBI is significantly enhanced in sedentary compared to physically active counterparts.