4.2 Article

The role of sleep deprivation in streptozotocin-induced Alzheimer's disease-like sporadic dementia in rats with respect to the serum level of oxidative and inflammatory markers

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EXPERIMENTAL BRAIN RESEARCH
卷 240, 期 12, 页码 3259-3270

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SPRINGER
DOI: 10.1007/s00221-022-06471-y

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Sleep deprivation (SD); Streptozotocin (STZ); Spatial memory; Inflammation; Oxidative stress

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Sleep deprivation can have both positive and negative effects on memory, depending on the duration. Long-term sleep deprivation impairs spatial learning and memory, decreases antioxidant activity, and increases inflammation. On the other hand, short-term sleep deprivation slightly improves spatial memory and significantly enhances antioxidant activity. Further studies are needed to explore the potential therapeutic effects of sleep deprivation on memory function, oxidative stress, and inflammation.
Numerous studies have shown the deleterious effects of sleep deprivation (SD) on memory. However, SD in various durations may induce different effects. Studies have reported that short-term or acute SD can improve cognitive functions. In addition, streptozotocin (STZ) significantly impairs learning and memory, and induces inflammation and oxidative stress. In this study, we aimed to investigate the effect of two types of SD (short term: 6 h; long term: 24 h) on STZ-induced spatial memory impairment in rats, with respect to the serum level of catalase (CAT), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1beta (IL-1 beta). Morris water maze apparatus was used to assess spatial memory performance and STZ was injected i.c.v., twice, and at the dose of 3 mg/kg, at an interval of 48 h. The results showed that only 24 h SD impaired spatial learning and memory in rats. In addition, 24 h SD attenuated anti-oxidant activity and increased the level of pro-inflammatory markers in the serum. STZ impaired spatial learning and memory, and attenuated anti-oxidant activity and increased the level of pro-inflammatory markers in the serum of rats. Furthermore, 6 h SD slightly and partially improved spatial memory and significantly improved anti-oxidant activity in rats, with no effect on STZ-induced inflammation. We suggest that STZ has more important mechanisms that are involved in its memory impairment effect, and maybe, STZ-induced inflammation has a more important role. We also suggest more detailed studies to investigate the potential therapeutic effect of SD (in different durations) on memory function, oxidative stress, and inflammation.

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