O papel da enzima Na+,K+-ATPase no déficit cognitivo e no efeito profilático induzido pelo exercício físico após o traumatismo crânio-encefálico

Abstract

Traumatic Brain Injury (TBI) is the major cause of death or cognitive deficits in industrialized countries. Although studies have indicate that the oxidative stress and functional deficits after TBI are connected events, the mechanisms that outline the development of these cognitive deficits are, still, limited. In this context, we investigated the involvement of oxidative stress markers (thiobarbituric acid reactive species; TBARS and protein carbonylation) and the Na+,K+-ATPase enzyme activity on the spatial learning after one and three months from a fluid percussion injury (FPI) in rats. The results revealed that FPI increase the latency of escape and the number of the errors on the Barnes Maze Test one and three months after FPI. We also found an increase of TBARS and protein carbonylation in parietal cortex after one and three months FPI. In addition, statistical analysis revealed a decrease of the Na+,K+- ATPase enzyme activity in the parietal cortex after FPI (time-dependent). These results suggest that cognitive impairment following FPI may result, at least in part, from increase of two oxidative stress markers, protein carbonylation and TBARS that occurs concomitantly to a decrease in Na+,K+-ATPase activity. Physical exercise, despite the involvement on the generation of the reactive oxygen species (ROS), is used on the rehabilitation of TBI. However, although the favorable effects of physical exercise on traumatic brain injury (TBI) patients is well known, the specific mechanisms involved in this protection after TBI has been limited. Thus, we investigated whether physical training protects against oxidative damage (measured by protein carbonylation and TBARS) and neurochemical alterations represented by immunodetection of alpha subunit and activity of Na+,K+-ATPase after FPI in cerebral cortex of rats. The results revealed that physical training protected against oxidative damage induced by FPI. In addition, physical training was effective against Na+,K+- ATPase enzyme activity inhibition and α subunit level decrease after FPI. The Pearson correlation showed that the decrease of the catalytical levels of the Na+,K+- ATPase enzyme α subunit is related with the increasing on oxidative stress markers. Moreover, the physical activity-related protection against free radicals induced by FPI links with maintenance of α subunit immunocontent. These results suggest that the effective protection stimulated by physical exercise on the neuronal damage induced by TBI has connection with the protection of the specific targets from the free radicals action, like Na+,K+-ATPase enzyme.