Lima Frederico Diniz, Souza Mauren Assis, Furian Ana Flávia, Rambo Leonardo Magno, Ribeiro Leandro Rodrigo, Martignoni Felipe Villa, Hoffmann Maurício Scopel, Fighera Michele Rechia, Royes Luiz Fernando Freire, Oliveira Mauro Schneider, de Mello Carlos Fernando
Centro de Ciências da Saúde, Laboratorio de Psicofarmacologia e Neurotoxicidade, Departamento de Fisiologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.
Behav Brain Res. 2008 Nov 21;193(2):306-10. doi: 10.1016/j.bbr.2008.05.013. Epub 2008 May 23.
Traumatic brain injury (TBI) is a devastating disease that commonly causes persistent mental disturbances and cognitive deficits. Although studies indicate that oxidative stress and functional deficits occurring after TBI are interrelated events, the knowledge of the mechanisms underlying the development of such cognitive deficits has been limited. Thus, in the present study, we investigated the effect of fluid percussion brain injury (FPI) on a spatial learning task and levels of oxidative stress markers, namely, protein carbonylation and thiobarbituric acid-reactive substances (TBARS) and Na+,K+-ATPase activity 1 or 3 months after FPI in rats. Statistical analysis revealed that FPI increased the scape latency and mean number of error in Barnes maze test 1 and 3 months after FPI. We also found that protein carbonylation and TBARS content increased in the parietal cortex 1 and 3 months after FPI. In addition, 3 months after FPI, protein carbonylation levels increased both in ipsilateral and contralateral cortices of FPI animals. Indeed, statistical analysis revealed a decrease in Na+,K+-ATPase activity in the cerebral cortex of 1 month FPI animals. Furthermore, the decrease in enzyme activity found 3 months was larger, when compared with 1 month after FPI. These results suggest that cognitive impairment following TBI 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.
创伤性脑损伤（TBI）是一种破坏性疾病，通常会导致持续性精神障碍和认知缺陷。尽管研究表明TBI后发生的氧化应激和功能缺陷是相互关联的事件，但对于此类认知缺陷发生发展的潜在机制的了解仍然有限。因此，在本研究中，我们调查了液压冲击脑损伤（FPI）对大鼠FPI后1个月或3个月空间学习任务以及氧化应激标志物水平的影响，这些标志物包括蛋白质羰基化、硫代巴比妥酸反应性物质（TBARS）以及Na +，K + -ATP酶活性。统计分析显示，FPI后1个月和3个月，FPI增加了Barnes迷宫试验中的逃避潜伏期和平均错误次数。我们还发现，FPI后1个月和3个月，顶叶皮质中的蛋白质羰基化和TBARS含量增加。此外，FPI后3个月，FPI动物同侧和对侧皮质中的蛋白质羰基化水平均升高。实际上，统计分析显示1个月FPI动物大脑皮质中Na +，K + -ATP酶活性降低。此外，与FPI后1个月相比，3个月时发现的酶活性降低幅度更大。这些结果表明，TBI后的认知障碍可能至少部分是由于两种氧化应激标志物蛋白质羰基化和TBARS的增加以及伴随Na +，K + -ATP酶活性降低而导致的。
