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<p>Evidence demonstrates that sleep deprivation (SD) impairs memory, cognitive function, and mood state. The disruption of the circadian rhythm induced by SD during the REM phase (REM-SD) leads to oxidative stress, neuroinflammation, and apoptosis proportional to the duration of the deprivation, but the underlying mechanisms remain largely unknown. Caffeine, which has neuroprotective effects, could prove beneficial in mitigating the effects of SD. In the present study, using the MMPM model, we investigate the neuroprotective effects of caffeine in rats subjected to REM-SD and elucidate the underlying mechanisms. Rats received caffeine (0.3&#xa0;g/l) during 5&#xa0;weeks of REM-SD. We then assessed affective and cognitive functions using behavioral tests. We evaluated blood levels of hs-CRP and CORT, as well as AchE, LDH activity, and oxidative stress markers in the HP, PFC, and HYP. Therefore, histological staining of these brain structures was examined. Caffeine treatment significantly improved memory and cognitive function in rats subjected to REM-SD. The study also showed that caffeine reduces hs-CRP, attenuates SD-induced HPA axis hyperactivation, decreases markers of oxidative stress, and enhances antioxidant defenses. Importantly, caffeine treatment modulates the cholinergic system, prevents neuronal lysis, and preserves neuronal density and architecture. The findings suggest that caffeine exerts neuroprotective, anti-inflammatory, antioxidant, and cytoprotective effects by preserving neuronal architecture against the effects of SD.</p>

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Caffeine treatment modulates neuronal density and oxidative stress pathway to preserve mood state and memory function in sleep-deprived rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • Wissal Baghdad,
  • Mohamed Yassine El Brouzi,
  • Oumaima Abouyaala,
  • Laila Ibouzine-Dine,
  • Marouane El Arbaoui,
  • Fatima Ezzahra El-Khiraoui,
  • Noura Rhmouny,
  • Hamza Lahrour,
  • Amal Satté,
  • Youssef Houssaini Squalli,
  • Abdelhalem Mesfioui,
  • Aboubaker El Hessni

摘要

Evidence demonstrates that sleep deprivation (SD) impairs memory, cognitive function, and mood state. The disruption of the circadian rhythm induced by SD during the REM phase (REM-SD) leads to oxidative stress, neuroinflammation, and apoptosis proportional to the duration of the deprivation, but the underlying mechanisms remain largely unknown. Caffeine, which has neuroprotective effects, could prove beneficial in mitigating the effects of SD. In the present study, using the MMPM model, we investigate the neuroprotective effects of caffeine in rats subjected to REM-SD and elucidate the underlying mechanisms. Rats received caffeine (0.3 g/l) during 5 weeks of REM-SD. We then assessed affective and cognitive functions using behavioral tests. We evaluated blood levels of hs-CRP and CORT, as well as AchE, LDH activity, and oxidative stress markers in the HP, PFC, and HYP. Therefore, histological staining of these brain structures was examined. Caffeine treatment significantly improved memory and cognitive function in rats subjected to REM-SD. The study also showed that caffeine reduces hs-CRP, attenuates SD-induced HPA axis hyperactivation, decreases markers of oxidative stress, and enhances antioxidant defenses. Importantly, caffeine treatment modulates the cholinergic system, prevents neuronal lysis, and preserves neuronal density and architecture. The findings suggest that caffeine exerts neuroprotective, anti-inflammatory, antioxidant, and cytoprotective effects by preserving neuronal architecture against the effects of SD.