ArticleBioengineered2021
The mechanism of sevoflurane post-treatment alleviating hypoxic-ischemic encephalopathy by affecting histone methyltransferase G9a in rats.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- G9a Targeting by miR-122 Ameliorates Ischemic Brain Injury via Enhanced Microglial Autophagy and Suppressed Ferroptosis.Neurochemical research · 2026Article
- Cerebral Inhibition of the H3K9 Methylation Could Ameliorate Blood-Brain Barrier Dysfunction and Neural Damage in Vascular Dementia.Archives of Razi Institute · 2024Article
- EHMT2 affects microglia polarization and aggravates neuronal damage and inflammatory response via regulating HMOX1.Translational neuroscience · 2023Article
- H3K9me2 regulation of BDNF expression via G9a partakes in the progression of heart failure.BMC cardiovascular disorders · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxic-ischemic encephalopathy (HIE) is recognized as the main cause of neonatal death, and efficient treatment strategies remain limited. This study aims to investigate the mechanism of sevoflurane (SF) post-treatment in alleviating HIE in rats. The HIE rat model and oxygen-glucose deprivation (OGD) cell model were established, and adeno-associated virus (AAV)-histone-lysine N-methyltransferase EHMT2 (G9a) was transfected after SF treatment. The learning and memory ability and the levels of nerve growth factor (NGF)/brain-derived neurotrophic factor (BDNF) were evaluated and determined. The levels of G9a/histone H3 lysine 9 dimethylation (H3K9me2) and the enrichment level of H3K9me2 in the promoter region of BDNF gene were analyzed. After SF post-treatment, the neurons in cerebral cortex, the learning and memory skills and the contents of NGF/BDNF were increased, while the apoptosis and G9a/H3K9me2 levels were reduced. After overexpression of G9a
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