Biochemistry study of brain damages in sleep deprivation rat

ObjectiveTo explore the biochemistry mechanism of brain damage in sleep deprivation (SD). MethodsThirty Sprague-Dawley male rats were randomly divided into 5 groups, one housed in normal cages (NC), one in tanks with large platforms (TC). The other three groups were SD model induced by the "Flower Pot" technique, and received 1-, 3-, and 5-days SD, respectively. Serum cortisol and IL-1β and IL-2 were measured with double antibodies radio-immune assay, and myelin basic protein (MBP) with enzyme linked immunoabsorbent assay. Nitric oxide (NO) levels and superoxide dismutase (SOD) activity in front cortex, hippocampus, midbrain, and hypothalamus were assayed. ResultsNO levels in frontal cortex, hippocampus, midbrain were different significantly between TC\ NC\ SD1 d\ SD3 d\ SD5 d group. SOD activity in frontal cortex, hippocampus, midbrain, and hypothalamus were also significantly different between TC\NC\ SD1 d\ SD3 d\ SD5 d group ( P 0.01). Serum levels of cortisol, MBP, IL-1β, and IL-2in SD5 d group were higher than that in TC and NC groups ( P 0.01, andP 0.05). Conclusions The resultsindicate that the brain damages after SD may be related to some biochemical varieties such as cortisol, NO, oxygen-derived free radicals, cytokine, and demyelination as well.