下调和上调
神经毒性
化学
活性氧
基因敲除
丙二醛
细胞生物学
谷胱甘肽
神经保护
氧化应激
毒性
药理学
生物化学
生物
细胞凋亡
有机化学
基因
酶
作者
Yu-Hui Tang,Lei Wu,Honglin Huang,Panpan Zhang,Wei Zou,Xiao‐Qing Tang,Yiyun Tang
出处
期刊:Toxicology
[Elsevier]
日期:2023-04-26
卷期号:491: 153517-153517
被引量:9
标识
DOI:10.1016/j.tox.2023.153517
摘要
Formaldehyde (FA) has neurotoxic characteristics and causes neurodegenerative disease. Our previous study demonstrated the neuroprotective effects of hydrogen sulfide (H2S) on FA-induced neurotoxicity in HT22 cells. Emerging evidence have supported that ferroptosis is involved in FA-induced neurotoxicity. To understand the mechanism of the protection of H2S against FA-induced neurotoxicity, this study explored the regulatory effect of H2S on FA-induced ferroptosis and the underlying mechanisms. We found that H2S (100, 200, and 400 μM, 30 min) reverses the ferroptosis induced by FA (100 μM, 24 h) in HT22 cells (a cell line of mouse hippocampal neurons), including decreases in free iron, reactive oxygen species (ROS), 4-hydroxy-2-trans-nominal (4-HNE), and malondialdehyde (MDA) contents, as well as an increase in glutathione (GSH) content. H2S (100, 200, and 400 μM, 30 min) also inhibited ferritinaphagy in FA-exposed HT22 cells, as evidenced by the downregulation of the ferritinophagy receptor nuclear receptor coactivator 4 (NCOA4) and microtubule-associated protein 1 light chain-3B (LC3B) as well as the upregulation of the main iron storage protein ferritin heavy chain 1 (FTH1) and p62. H2S (100, 200, and 400 μM, 30 min) also up-regulated the expression of growth differentiation factor-11 (GDF11) in FA-exposed HT22 cells. Furthermore, knockdown of GDF11 in HT22 cells cancelled the beneficial effects of H2S on FA-induced ferroptosis and ferritinaphagy. These data indicated that the protective mechanism underlying H2S-prevented neurotoxicity of FA is involved in alleviating FA-induced ferroptosis via inhibiting ferritinaphagy by upregulation of GDF11.
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