A Review on Pathophysiological Aspects of Sleep Deprivation

Agrawal, Shelly; Singh, Vishesh; Singh, Charan; Singh, Arti

doi:10.2174/1871527321666220512092718

Cited by 6 publications

(5 citation statements)

References 147 publications

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“…Here, we found increased activation of microglia in spinal cord of SD mice, which indicated that inflammatory reaction occurred after SD exposure. Also, SD is capable of affecting DNA integrity by prolonging oxidative stress [30][31][32]. It causes singlestrand breaks by attacking deoxyribose through excessively produced ROS.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment of the ROS Inhibitor Phenyl-N-tert-butylnitrone Alleviates Sleep Deprivation-Induced Hyperalgesia by Suppressing Microglia Activation and NLRP3 Inflammasome Activity in the Spinal Dorsal Cord

et al. 2022

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Sleep deprivation, a common perioperative period health problem, causes ocular discomfort and affects postsurgical pain. However, the mechanism of sleep deprivation-induced increased pain sensitivity is elusive. This study aims to explore the role of ROS in sleep deprivation (SD)-induced hyperalgesia and the underlying mechanism. A 48-h continuous SD was performed prior to the hind paw incision pain modeling in mice. We measured ROS levels, microglial activation, DNA damage and protein levels of iNOS, NLRP3, p-P65 and P65 in mouse spinal dorsal cord. The involvement of ROS in SD-induced prolongation of postsurgical pain was further confirmed by intrathecal injection of ROS inhibitor, phenyl-N-tert-butylnitrone (PBN). Pretreatment of 48-h SD in mice significantly prolonged postsurgical pain recovery, manifesting as lowered paw withdrawal mechanical threshold and paw withdrawal thermal latency. It caused ROS increase and upregulation of iNOS on both Day 1 and 7 in mouse spinal dorsal cord. In addition, upregulation of NLRP3 and p-P65, microglial activation and DNA damage were observed in mice pretreated with 48-h SD prior to the incision. Notably, intrathecal injection of PBN significantly reversed the harmful effects of SD on postsurgical pain recovery, hyperalgesia, microglial activation and DNA damage via the NF-κB signaling pathway. Collectively, ROS increase is responsible for SD-induced hyperalgesia through activating microglial, triggering DNA damage and enhancing NLRP3 inflammasome activity in the spinal dorsal cord.

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Section: Discussionmentioning

confidence: 99%

Pretreatment of the ROS Inhibitor Phenyl-N-tert-butylnitrone Alleviates Sleep Deprivation-Induced Hyperalgesia by Suppressing Microglia Activation and NLRP3 Inflammasome Activity in the Spinal Dorsal Cord

et al. 2022

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“…PI3K/AKT/BDNF signaling is closely related to the central system disease, psychiatric disease, and sleep disorders [26,27]. Therefore, the transduction of the PI3K/AKT/BDNF signaling in the brain tissues of rats was finally examined.…”

Section: Resultsmentioning

confidence: 99%

“…PI3K/AKT/BDNF signaling is closely related to the central system disease, psychiatric disease, and sleep disorders [26,27,34]. The activation of PI3K/AKT signaling is discovered to be blocked in mice undergoing sleep deprivation [35].…”

Section: Discussionmentioning

confidence: 99%

“…In this research, Sophora flavescens alcohol extract upregulated 5-HT and 5-HIAA levels, while downregulating NE and DA levels in insomnia model rats, and the regulatory role of Sophora flavescens alcohol extract in 5-HA, HIAA, NE, and DA levels is similar with that of positive control drug ZRAS, further demonstrating the anti-insomnia effect of Sophora flavescens alcohol extract. PI3K/AKT/BDNF signaling is closely related to the central system disease, psychiatric disease, and sleep disorders [26,27,34]. The activation of PI3K/AKT signaling is discovered to be blocked in mice undergoing sleep deprivation [35].…”

Section: Discussionmentioning

confidence: 99%

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Sophora flavescens alcohol extract ameliorates insomnia and promotes PI3K/AKT/BDNF signaling transduction in insomnia model rats

Wu,

Yao,

Zhang

et al. 2024

NeuroReport

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Active ingredient of Sophora flavescens is reported to promote non-rapid eye movement (NREM) sleep. However, the role of Sophora flavescens alcohol extract in insomnia is elusive, which is addressed in this study, together with the exploration on its potential mechanism. An insomnia model of rats was established by para-chlorophenylalanine induction and further treated with SFAE or Zaoren Anshen capsule (ZRAS; positive control drug). Sleep quality and sleep architecture of rats were evaluated by the sleep test, electroencephalogram and electromyogram. The levels of monoamine neurotransmitters in rat hypothalamus were determined using ELISA, and the transduction of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/brain-derived neurotrophic factor (BDNF) signaling in the brain tissues of rats was examined by Western blot. SFAE and ZRAS increased the sleeping time and decreased the sleep latency of insomnia rats. SFAE reduced waking time and increased NREM and REM time, while changing power density of wakefulness, NREM sleep, and REM sleep in insomnia rats. SFAE and ZRAS upregulated levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid, and downregulated those of norepinephrine and dopamine in insomnia rats. Besides, SFAE and ZRAS elevated BDNF expression as well as the ratios of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT. The role of SFAE in insomnia model rats was similar with that of ZRAS. SFAE reduces insomnia and enhances the PI3K/AKT/BDNF signaling transduction in insomnia model rats, which can function as a drug candidate for insomnia.

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“…Animals also experience learning and memory problems after REM sleep deprivation [9]. However, the mechanism is still inconclusive [10]. At present, sedative and hypnotic drugs, such as benzodiazepines [11], zolpidem [12] and selective serotonin reuptake inhibitors trazodone, agomelatine and mirtazapine [13,14], are widely used to improve sleep problems.…”

Section: Introductionmentioning

confidence: 99%

Gastrodin Improves Cognitive Dysfunction in REM Sleep-Deprived Rats by Regulating TLR4/NF-κB and Wnt/β-Catenin Signaling Pathways

Liu

et al. 2023

Brain Sciences

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Gastrodin is the active ingredient in Gastrodia elata. Our previous studies demonstrated that gastrodin ameliorated cerebral ischemia–reperfusion and hypoperfusion injury and improved cognitive deficit in Alzheimer’s disease. This study aims to examine the effects of gastrodin on REM sleep deprivation in rats. Gastrodin (100 and 150 mg/kg) was orally administered for 7 consecutive days before REM sleep deprivation. Seventy-two hours later, pentobarbital-induced sleep tests and a Morris water maze were performed to measure REM sleep quality and learning and memory ability. Histopathology was observed with hematoxylin–eosin staining, and the expression of the NF-κB and Wnt/β-catenin signaling pathways was examined using Western blot. After REM sleep deprivation, sleep latency increased and sleep duration decreased, and the ability of learning and memory was impaired. Neurons in the hippocampal CA1 region and the cortex were damaged. Gastrodin treatment significantly improved REM sleep-deprivation-induced sleep disturbance, cognitive deficits and neuron damage in the hippocampus CA1 region and cerebral cortex. A mechanism analysis revealed that the NF-κB pathway was activated and the Wnt/β-catenin pathway was inhibited after REM sleep deprivation, and gastrodin ameliorated these aberrant changes. Gastrodin improves REM sleep-deprivation-induced sleep disturbance and cognitive dysfunction by regulating the TLR4/NF-κB and Wnt/β-catenin signaling pathways and can be considered a potential candidate for the treatment of REM sleep deprivation.

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A Review on Pathophysiological Aspects of Sleep Deprivation

Cited by 6 publications

References 147 publications

Pretreatment of the ROS Inhibitor Phenyl-N-tert-butylnitrone Alleviates Sleep Deprivation-Induced Hyperalgesia by Suppressing Microglia Activation and NLRP3 Inflammasome Activity in the Spinal Dorsal Cord

Pretreatment of the ROS Inhibitor Phenyl-N-tert-butylnitrone Alleviates Sleep Deprivation-Induced Hyperalgesia by Suppressing Microglia Activation and NLRP3 Inflammasome Activity in the Spinal Dorsal Cord

Sophora flavescens alcohol extract ameliorates insomnia and promotes PI3K/AKT/BDNF signaling transduction in insomnia model rats

Gastrodin Improves Cognitive Dysfunction in REM Sleep-Deprived Rats by Regulating TLR4/NF-κB and Wnt/β-Catenin Signaling Pathways

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