ArticleMolecular neurobiology2025
Myricetin Mitigated Sevoflurane-induced Cognitive Dysfunction in Aged-mice Through Inhibiting Histone Deacetylase 2/nuclear Factor Erythroid 2-related Factor 2/heme Oxygenase-1 Signalling-mediated Ferroptosis and Mitochondrial Dysfunction.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Fat on Fire: Disrupted Microglial Lipid Metabolism as a Driver of Anesthetic Neurotoxicity.Neuroscience bulletin · 2026Review
- DDIT4 silencing attenuates sevoflurane-induced ferroptosis via the mTOR pathway in neuronal cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Histone H3K18 Lactylation Contributes to Perioperative Neurocognitive Disorder Through Immune Checkpoint Lymphocyte Activation Gene 3 Mediated Microglial Pyroptosis.CNS neuroscience & therapeutics · 2026Article
- Exploring Sevoflurane promotes hippocampal neuron mitophagy in elderly postoperative cognitive dysfunction by HSP90AA1 based on network pharmacology.Experimental brain research · 2026Article
- Natural Small Molecules Targeting Oxidative Stress and Redox Homeostasis in Aging: Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
- Ferroptosis: an emerging key mechanism linking aging, surgical and anesthetic exposure to postoperative cognitive dysfunction.Frontiers in immunology · 2026Review
- Multi-omics profiling reveals mitochondrial dysfunction and epigenetic dysregulation in postoperative cognitive dysfunction: identification of novel biomarkers in an aged mouse model.Biogerontology · 2025Article
- Deciphering sevoflurane-induced neurotoxicity: from isolated targets to intricate regulatory networks.Frontiers in neuroscience · 2025Review
- Ferroptosis in neurodegenerative diseases: potential mechanisms of exercise intervention.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
6 authors.
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Abstract
Sevoflurane anaesthesia induces neurotoxicity and postoperative cognitive dysfunction (POCD) after surgery. This study investigated the roles and potential mechanisms of the natural flavonoid myricetin in sevoflurane-induced cognitive dysfunction. Primary hippocampal neurons were treated with 3% sevoflurane to establish a neuron injury model. Neurons was pre-treated with different concentrations of myricetin, and ferroptosis inhibitor ferrostatin-1 (Fer-1) was used as a positive control. Moreover, mice were anaesthetised with 3% sevoflurane to establish an in-vivo model, and they were pre-treated with 50 or 100 m/kg myricetin. Cell viability and death were determined. Ferroptosis-related markers, including intracellular iron content, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), 4-hydroxy-2-nonenal (4-HNE), glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) protein levels were measured. Myricetin treatment enhanced cell viability and mitigated sevoflurane-induced cell death in the hippocampal neurons. Sevoflurane exposure increased the ROS, MDA and 4-HNE levels and reduced the GSH level, whereas myricetin treatment abrogated these effects. Meanwhile, myricetin treatment restrained sevoflurane-induced increase in intracellular iron content and GPX4 and SLC7A11 protein levels. A high dose of myricetin showed distinct protective effects. Mechanistic studies demonstrated that myricetin treatment reversed sevoflurane-induced histone deacetylase 2 (HDAC2) upregulation and nuclear factor erythroid 2-related factor 2 (Nrf2) deacetylation, thus activating the Nrf2/heme oxygenase-1 (HO-1) signalling. Myricetin treatment mitigated sevoflurane-induced cognitive dysfunction in aged mice by inhibiting hippocampal ferroptosis and mitochondrial dysfunction via the HDAC2/Nrf2/HO-1 signalling pathway. Myricetin may be a treatment option for POCD after surgery.
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