ArticleBioengineered2021
Sevoflurane induces inflammation in primary hippocampal neurons by regulating Hoxa5/Gm5106/miR-27b-3p positive feedback loop.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Genetic Assessment of Neurotoxicity Accompanied by Inhalational Anesthesia in Preclinical Studies with Focus on Sevoflurane and Isoflurane-A Narrative Review.Brain sciences · 2026Review
- Advances in the Mechanism of ceRNA Regulation in Postoperative Cognitive Dysfunction.Current neuropharmacology · 2026Review
- Effects of volatile and intravenous anesthetics on postoperative cognitive dysfunction: a mechanistic review.Journal of anesthesia · 2025Review
- Common and distinct circulating microRNAs in four neurovascular disorders.Biochemistry and biophysics reports · 2025Article
- Suppression of mPFC-Amygdala Circuit Mitigates Sevoflurane-Induced Cognitive Deficits in Aged Mice.CNS neuroscience & therapeutics · 2025Article
- lncRNA PART1 improves sevoflurane-induced impairments in learning and cognitive function by regulating miR-16-5p expression and reducing neuroinflammation.Toxicology research · 2025Article
- The role of sevoflurane in postoperative cognitive dysfunction.Medical gas research · 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
- Sequencing Reveals miRNAs Enriched in the Developing Mouse Enteric Nervous System.Non-coding RNA · 2023Article
- The circular RNANeural regeneration research · 2023Article
- Recent progress on the role of non-coding RNA in postoperative cognitive dysfunction.Frontiers in cellular neuroscience · 2022Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postoperative cognitive dysfunction (POCD) is a normal condition that develops after surgery with anesthesia, leading to deterioration of cognitive functions. However, the mechanism of POCD still remains unknown. To elucidate the POCD molecular mechanism, sevoflurane was employed in the present study to generate neuroinflammation mice model. Sevoflurane treatment caused inflammatory markers IL6, IL-10 and TNF-α high expression in primary hippocampal neurons and blood samples. Long non-coding RNA Gm5106 was found to be increased after being stimulated with sevoflurane. Silencing Gm5106 inhibited neuron inflammation. In the meanwhile, Gm5106 was identified as a direct target of miR-27b-3p that was inhibited by sevoflurane and related to inflammation suppression. In addition, transcription factor (TF) Hoxa5 was validated to activate Gm5106 through two binding motifs in the promoter region after sevoflurane exposure. Furthermore, miR-27b-3p also directly targeted Hoxa5 3'UTR, which affected nuclear Hoxa5 protein served as TF. Hoxa5 protein instead of 3'UTR reduced miR-27b-3p, in which Gm5106 knocking down abrogated this effect. In conclusion, sevoflurane induces neuroinflammation through increasing long non-coding RNA Gm5106, which is transcriptionally activated by Hoxa5 and directly targeted by miR-27-3p. Apart from that, Hoxa5, Gm5106, and miR-27b-3p form a positive feedback loop in sevoflurane stimulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.