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2000
Volume 19, Issue 6
  • ISSN: 1567-2050
  • E-ISSN: 1875-5828

Abstract

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.

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/content/journals/car/10.2174/1567205019666220805092450
2022-05-01
2025-04-15
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  • Article Type:
    Research Article
Keyword(s): brain derived neurotrophic factor; catalase; glutathione; maze; Sage; sleep deprivation
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