ArticleMolecular neurobiology2022
Sevoflurane Offers Neuroprotection in a Cerebral Ischemia/Reperfusion Injury Rat Model Through the E2F1/EZH2/TIMP2 Regulatory Axis.
Article in Molecular neurobiology, 2022. 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, 19 citations in OpenAlex.
- Effects of E2F1 Point Acetylation at Lysine 117 or 125 on Neuronal Apoptosis After Ischemic Injury.Neurochemical research · 2025Article
- E2F1/CDK5/DRP1 axis mediates microglial mitochondrial division and autophagy in the pathogenesis of cerebral ischemia-reperfusion injury.Clinical and translational medicine · 2025Article
- Inhaled Anesthetics: Beyond the Operating Room.Journal of clinical medicine · 2024Review
- GSK-126 Attenuates Cell Apoptosis in Ischemic Brain Injury by Modulating the EZH2-H3K27me3-Bcl2l1 Axis.Molecular neurobiology · 2024Article
- Pharmacological inhibition of EZH2 using a covalent inhibitor suppresses human ovarian cancer cell migration and invasion.Molecular and cellular biochemistry · 2024Article
- Long-term sevoflurane exposure relieves stress-enhanced fear learning and anxiety in PTSD mice.Translational neuroscience · 2023Article
- A retrospect and outlook on the neuroprotective effects of anesthetics in the era of endovascular therapy.Frontiers in neuroscience · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia/reperfusion (I/R) injury contributes considerably to the poor prognosis in patients with ischemic stroke. This study is aimed to delineate the molecular mechanistic actions by which sevoflurane protects against cerebral I/R injury. A rat model of cerebral I/R injury was established and pre-treated with sevoflurane, in which hippocampal neuron apoptosis was found to be repressed and the level of E2F transcription factor 1 (E2F1) was observed to be down-regulated. Then, the up-regulated expression of E2F1 was validated in rats with cerebral I/R injury, responsible for stimulated neuron apoptosis. Further, the binding of E2F1 to enhancer of zeste homolog 2 (EZH2) and EZH2 to tissue inhibitor of metalloproteinases-2 (TIMP2) was identified. The stimulative effect of the E2F1/EZH2/TIMP2 regulatory axis on neuron apoptosis was subsequently demonstrated through functional assays. After that, it was substantiated in vivo that sevoflurane suppressed the apoptosis of hippocampal neurons in rats with cerebral I/R injury by down-regulating E2F1 to activate the EZH2/TIMP2 axis. Taken together, our data elucidated that sevoflurane reduced neuron apoptosis through mediating the E2F1/EZH2/TIMP2 regulatory axis, thus protecting rats against cerebral I/R injury.
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