ArticleNeurochemical research2021
LncRNA Neat1/miR-298-5p/Srpk1 Contributes to Sevoflurane-Induced Neurotoxicity.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Evaluation of neurotoxicity of drugs from morphological and electrophysiological endpoints using human iPSC-derived neural cell models.Frontiers in cellular and infection microbiology · 2026Article
- The Preconditioning with Sevoflurane Alleviates Hypoxia-Reoxygenation-Induced Myocardial Cell Injury by Regulating the lncRNA LINC00265/miR-370-3p Axis.Cardiovascular toxicology · 2025Article
- lncRNA PART1 improves sevoflurane-induced impairments in learning and cognitive function by regulating miR-16-5p expression and reducing neuroinflammation.Toxicology research · 2025Article
- Possible Involvement of Hippocampal miR-539-3p/Lrp6/Igf1r Axis for Diminished Working Memory in Mice Fed a Low-Carbohydrate and High-Protein Diet.Molecular nutrition & food research · 2025Article
- KLF7 enhances the inflammatory response in LPS-induced alveolar epithelial cellsCentral-European journal of immunology · 2025Article
- Mechanistic insights into sevoflurane-induced hippocampal neuronal damage and cognitive dysfunction through the NEAT1/Nrf2 signaling axis in aged rats.Cell biology and toxicology · 2024Article
- Article
- Screening of potential biomarkers in propofol-induced neurotoxicity via bioinformatics prediction and experimental verification.American journal of translational research · 2024Article
- LncRNA SNHG3 Promotes Sevoflurane-Induced Neuronal Injury by Activating NLRP3 via NEK7.Neurochemical research · 2023Article
- Construction and analysis of circular RNA-associated competing endogenous RNA network in the hippocampus of aged mice for the occurrence of postoperative cognitive dysfunction.Frontiers in aging neuroscience · 2023Article
- Effects of lncRNA HOXA11-AS on Sevoflurane-Induced Neuronal Apoptosis and Inflammatory Responses by Regulating miR-98-5p/EphA4.Mediators of inflammation · 2023Article
- Sevoflurane reverses cisplatin resistance in neuroblastoma cells through the linc00473/miR-490-5p/AKT1 axis.Saudi medical journal · 2022Article
- Sevoflurane anesthesia ameliorates LPS-induced acute lung injury (ALI) by modulating a novel LncRNA LINC00839/miR-223/NLRP3 axis.BMC pulmonary medicine · 2022Article
- Research progress on molecular mechanisms of general anesthetic-induced neurotoxicity and cognitive impairment in the developing brain.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sevoflurane is a widely used volatile anesthetic, that can cause long-term neurotoxicity and learning and memory impairment. Long non-coding RNAs (lncRNAs) have been demonstrated to function as key mediators in neurotoxicity. This study aimed to investigate the effects of lncRNA Neat1 on sevoflurane-induced neurotoxicity. The expression of Neat1, miR-298-5p, and Srpk1 was measured by RT-qPCR. Cell viability, cell apoptosis, inflammation markers, and reactive oxygen species (ROS) generation were examined by CCK-8, TUNEL, ELISA, and the ROS kit. The interaction between miR-298-5p and Neat1 or Srpk1 was confirmed by luciferase reporter assay. In our study, it was found that sevoflurane aggravated neurotoxicity through inhibiting cell viability and enhancing cell apoptosis, neuroinflammation, and ROS generation. Neat1 was up-regulated in sevoflurane-treated HT22 cells, and Neat1 knockdown improved sevoflurane-mediated neurotoxicity. Through the exploration of the ceRNA mechanism, we found that Neat1 bound with miR-298-5p, and Srpk1 was a direct target gene of miR-298-5p. Finally, rescue assays proved that up-regulation of Srpk1 reversed the effects of Neat1 knockdown on neurotoxicity. In conclusion, our study revealed that lncRNA Neat1 facilitated sevoflurane-stimulated neurotoxicity by sponging miR-298-5p to up-regulate Srpk1. These findings might provide novel insights into the treatment of sevoflurane-induced neurotoxicity.
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