ArticleKorean journal of anesthesiology2024
Damage-associated molecular patterns as a mechanism of sevoflurane-induced neuroinflammation in neonatal rodents.
Article in Korean journal of anesthesiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 4 citations in OpenAlex.
- Comment on "transmembrane protein 45b in peripheral sensory neurons selectively mediates IL-31-dependent chemical itch".Journal of anesthesia · 2026Article
- mExperimental & molecular medicine · 2026Article
- The NLRP3 Inflammasome: A Central Mediator in Sevoflurane-Induced Neurotoxicity and A Potential Target for Neuroprotection.Molecular neurobiology · 2026Review
- Damage-Associated Molecular Patterns in Perioperative Anesthesia Care: A Clinical Perspective.Anesthesia research · 2026Article
- Total intravenous anesthesia facilitates early cognitive recovery compared with inhalational anesthesia in Alzheimer's disease patients after cervical lymphatic-venous anastomosis: a randomized controlled trial.American journal of translational research · 2026Article
- Deciphering sevoflurane-induced neurotoxicity: from isolated targets to intricate regulatory networks.Frontiers in neuroscience · 2025Review
- Downregulation of circTLK1 improves the impairments in learning and memory induced by anesthetics via regulating miR-374b-5p expression and reducing neuroinflammation.Toxicology research · 2024Article
- Effects of Cohabitation on Neurodevelopmental Outcomes in Rats Discordant for Neonatal Exposure to Sevoflurane.Biological psychiatry global open science · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGeneral anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation.
methodsA three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay.
resultsIn total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels.
conclusionsIn conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.
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