ArticleJournal of neuroinflammation2022
The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed.
- Olfactory Mucosa MSCs-Derived Exosomal RPL6 Attenuates Seizure-Induced Neuronal Damage via FGF2-Mediated Oxidative Stress and Mitophagy.Neurochemical research · 2026Article
- Non-anesthetic Effects of Anesthetics and Organ Protection.Current neuropharmacology · 2026Review
- Ultrasound-activated piezoelectric nanostickers for neural stem cell therapy of traumatic brain injury.Nature materials · 2025Article
- Sevoflurane versus propofol on immediate postoperative cognitive dysfunction in patients undergoing cardiac surgery under cardiopulmonary bypass: a comparative analysis.Journal of cardiothoracic surgery · 2025Article
- Anesthetics in pathological cerebrovascular conditions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- Effects ofFrontiers in veterinary science · 2025Article
- Chaperone-Mediated Autophagy in Brain Injury: A Double-Edged Sword with Therapeutic Potentials.Molecular neurobiology · 2024Review
- Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats.International journal of molecular sciences · 2024Article
- Adiponectin deficiency is a critical factor contributing to cognitive dysfunction in obese mice after sevoflurane exposure.Molecular medicine (Cambridge, Mass.) · 2024Article
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- Evaluation of canine adipose-derived mesenchymal stem cells for neurological functional recovery in a rat model of traumatic brain injury.BMC veterinary research · 2024Article
- Involvement of Fgf2-mediated tau protein phosphorylation in cognitive deficits induced by sevoflurane in aged rats.Molecular medicine (Cambridge, Mass.) · 2024Article
- RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.CNS neuroscience & therapeutics · 2024Article
- Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury.Advanced healthcare materials · 2023Article
- Sevoflurane Preconditioning Alleviates Posttraumatic Stress Disorder-Induced Apoptosis in the Hippocampus via the EZH2-Regulated Akt/mTOR Axis and Improves Synaptic Plasticity.Journal of molecular neuroscience : MN · 2023Article
- Long-term sevoflurane exposure relieves stress-enhanced fear learning and anxiety in PTSD mice.Translational neuroscience · 2023Article
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10 authors.
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Abstract
backgroundTraumatic brain injury (TBI) is a kind of acquired brain injury, which is caused by external mechanical forces. Moreover, the neuroprotective role of sevoflurane (Sevo) has been identified in TBI. Therefore, this research was conducted to figure out the mechanism of Sevo in TBI via FGF2.
methodsThe key factors of neuroprotective effects of Sevo in TBI rats were predicted by bioinformatics analysis. A TBI model was induced on rats that then inhaled Sevo for 1 h and grouped via lentivirus injection. Modified Neurological Severity Score was adopted to evaluate neuronal damage in rats, followed by motor function and brain water content measurement. FGF2, EZH2, and HES1 expression in brain tissues was evaluated by immunofluorescence staining, and expression of related genes and autophagy factors by RT-qPCR and Western blot analysis. Methylation-specific PCR was performed to assess HES1 promoter methylation level, and ChIP assay to detect the enrichment of EZH2 in the HES1 promoter. Neuronal damage was assessed by cell immunofluorescence staining, and neuronal apoptosis by Nissl staining, TUNEL staining, and flow cytometry.
resultsSevo diminished brain edema, improved neurological scores, and decreased neuronal apoptosis and autophagy in TBI rats. Sevo preconditioning could upregulate FGF2 that elevated EZH2 expression, and EZH2 bound to the HES1 promoter to downregulate HES1 in TBI rats. Also, FGF2 or EZH2 overexpression or HES silencing decreased brain edema, neurological deficits, and neuronal autophagy and apoptosis in Sevo-treated TBI rats.
conclusionsOur results provided a novel insight to the neuroprotective mechanism of Sevo in TBI rats by downregulating HES1 via FGF2/EZH2 axis activation.
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