机制(生物学)
缺血性损伤
缺血
乙酰化
创伤性脑损伤
脑损伤
缺氧(环境)
氧化应激
神经科学
医学
麻醉
化学
生物
内科学
生物化学
氧气
基因
精神科
哲学
认识论
有机化学
作者
Xin Liu,Xuwei Tao,Zhen Xiong,Huizhen Wang,Linkong Zeng
出处
期刊:Brain Injury
[Taylor & Francis]
日期:2025-03-10
卷期号:39 (8): 635-645
被引量:3
标识
DOI:10.1080/02699052.2025.2468309
摘要
OBJECTIVE: We investigated the mechanism of histone deacetylase 2 (HDAC2) modulating nuclear factor erythroid 2-related factor 2 (Nrf2) acetylation level in neuronal ferroptosis of hypoxic-ischemic brain injury (HIBI) neonatal rats. METHODS: , Nrf2 acetylation, and nuclear Nrf2 in hippocampal tissues were determined. RESULTS: . Inhibition of HDAC2 partially ameliorated neuronal ferroptosis in HIBI neonatal rats. HDAC2 regulated Nrf2 expression and repressed Nrf2 nuclear translocation by mediating Nrf2 deacetylation. Inhibition of Nrf2 partially reversed the ameliorative effect of HDAC2 on neuronal ferroptosis in HIBI neonatal rats. CONCLUSION: HDAC2 modulated neuronal ferroptosis in HIBI neonatal rats by mediating Nrf2 deacetylation.
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