ArticleIranian journal of pharmaceutical research : IJPR2022
Amelioratory Effect of Melatonin on Cognition Dysfunction Induced by Sevoflurane Anesthesia in Aged Mice.
Article in Iranian journal of pharmaceutical research : IJPR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 11 citations in OpenAlex.
- Blood-brain barrier-penetrating Angiopep-2/Sirtuin 1 nanoparticles rescue sevoflurane neurotoxicity through multi-omics identified necroptosis pathways.Journal of nanobiotechnology · 2025Article
- Berberine Ameliorates Postoperative Cognitive Dysfunction in Aged Mice and Regulates the PI3K-AKT Pathway: A Network Pharmacology Study.Journal of cellular and molecular medicine · 2025Article
- Repeated sevoflurane exposure causes hypomyelination in the prefrontal cortex of adult male mice.Scientific reports · 2025Article
- Deciphering sevoflurane-induced neurotoxicity: from isolated targets to intricate regulatory networks.Frontiers in neuroscience · 2025Review
- The Inhibition of Reactive Oxygen Species Modulator 1 Attenuates Sevoflurane-Induced Neural Injury via Reducing Apoptosis and Oxidative Stress.Journal of molecular neuroscience : MN · 2024Article
- Efficacy of melatonin in alleviating disorders arising from repeated exposure to sevoflurane in males and females of the Wistar rats during preadolescence.Scientific reports · 2024Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Postoperative cognitive dysfunction (POCD) can be described as a clinical phenomenon characterized by cognitive impairment in patients, particularly elderly patients, after anesthesia and surgery. Researchers have focused on the probable effect of general anesthesia drugs on cognitive functioning status in older adults. Melatonin is an indole-type neuroendocrine hormone with broad biological activity and potent anti-inflammatory, anti-apoptotic, and neuroprotective effects. This study investigated the effects of melatonin on cognitive behavior in aged mice anesthetized with sevoflurane. In addition, melatonin's molecular mechanism was determined. Objectives: This study aimed to investigate the mechanisms of melatonin against sevoflurane-induced neurotoxicity. Methods: A total of 94 aged C57BL/6J mice were categorized into different groups, namely control (control + melatonin (10 mg/kg)), sevoflurane (sevoflurane + melatonin (10 mg/kg)), sevoflurane + melatonin (10 mg/kg) + phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) inhibitor LY294002 (30 mg/kg), and sevoflurane + melatonin (10 mg/kg) + mammalian target of rapamycin (mTOR) inhibitor (10 mg/kg). The open field and Morris water maze tests were utilized to assess the neuroprotective effects of melatonin on sevoflurane-induced cognitive impairment in aged mice. The expression levels of the apoptosis-linked proteins, PI3K/Akt/mTOR signaling pathway, and pro-inflammatory cytokines in the brain's hippocampus region were determined using the Western blotting technique. The apoptosis of the hippocampal neurons was observed using the hematoxylin and eosin staining technique. Results: Neurological deficits in aged, sevoflurane-exposed mice were significantly decreased after melatonin treatment. Mechanistically, melatonin treatment restored sevoflurane-induced down-regulated PI3K/Akt/mTOR expression and significantly attenuated sevoflurane-induced apoptotic cells and neuroinflammation. Conclusions: The findings of this study have highlighted the neuroprotective effect of melatonin on sevoflurane-induced cognitive impairment via regulating the PI3K/Akt/mTOR pathway, which might be effective in the clinical treatment of elderly patients with anesthesia-induced POCD.
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