Department of Medicinal Chemistry and Pharmacognosy, Faculty of Pharmacy, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110, Jordan.
Department of Pharmacy Practice and Pharmacotherapeutics, University of Sharjah, Sharjah, UAE.
Curr Alzheimer Res. 2022;19(6):440-448. doi: 10.2174/1567205019666220805092450.
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.
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.
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.
Chronic treatment with sage extract (S. Triloba) precluded SD-induced memory impairment by regularizing antioxidant parameters levels in rats' hippocampus.
学习和记忆缺陷与海马体的氧化损伤有关。此外，睡眠剥夺（SD）通过减轻氧化应激平衡来改善记忆。在本报告中，研究了口服鼠尾草（Salvia triloba）提取物对慢性 SD 引起的认知障碍的潜在神经保护作用。
采用改良的多平台（每天 8 小时；持续六周）方法诱导成年雄性 Wistar 大鼠发生 SD。同时，给予 S. triloba 提取物（375mg/kg，口服）持续六周。之后，利用放射臂水迷宫试验评估空间学习和记忆。此外，还测量了大鼠海马体中不同抗氧化参数的活性：谷胱甘肽过氧化物酶（GPx）、氧化型谷胱甘肽（GSSG）、还原型谷胱甘肽（GSH）、过氧化氢酶、超氧化物歧化酶（SOD）和硫代巴比妥酸反应物质（TBARS）。此外，还评估了脑源性神经营养因子（BDNF）的水平。
目前的结果表明，慢性 SD 显著损害了短期和长期记忆，而鼠尾草提取物抑制了这些后果。此外，鼠尾草提取物显著稳定了抗氧化酶水平，这些酶因 SD 而降低，如 SOD、过氧化氢酶和 GPx（P<0.05），并显著增加了 SD 大鼠的 GSH/GSSG 比值（P<0.05）。然而，鼠尾草提取物给药后，GSH、TBARS 或 BDNF 水平没有明显变化（P>0.05）。
慢性给予鼠尾草提取物（S. Triloba）可通过调节大鼠海马体中抗氧化参数水平来预防 SD 引起的记忆障碍。
