Assessing the Influence of on Memory Deficit Caused by Sleep Deprivation in the Context of Oxidative Stress.

BACKGROUND

Learning and memory deficit has been reported to be correlated to oxidative mutilation in the hippocampus. Moreover, sleep deprivation (SD) mitigates memory via distressing oxidative stress balance. In the current report, the prospective neuroprotective role of oral sage (Salvia triloba) extract on cognitive impairment induced by chronic SD was investigated.

METHODS

The SD was induced in adult male Wistar rats employing a modified multiple platform (8 h/day; for six weeks). Simultaneously, S. triloba extract (375 mg/kg, orally) was administered for six weeks. Thereafter, the Radial Arm Water Maze test was utilized to evaluate spatial learning and memory. Moreover, activities of different hippocampal antioxidant parameters: glutathione peroxidase (GPx), oxidized glutathione (GSSG), reduced glutathione (GSH), catalase, superoxide dismutase (SOD), and the thiobarbituric acid reactive substance (TBARS) were measured in rats' hippocampus. Moreover, the level of brain derived neurotrophic factor (BDNF) was assessed.

RESULTS

Current results illustrate that chronic SD significantly compromised both memories, shortand long-term, while sage extract inhibited these consequences. Moreover, sage extract remarkably stabilized the antioxidant enzyme levels, which were decreased by SD, such as: SOD, catalase, and GPx (P < 0.05), and remarkably augmented the GSH/GSSG ratio in SD rats (P < 0.05). However, no substantial alterations of GSH, TBARS or BDNF levels (P > 0.05) were seen with sage extract administration.

CONCLUSION

Chronic treatment with sage extract (S. Triloba) precluded SD-induced memory impairment by regularizing antioxidant parameters levels in rats' hippocampus.