ArticleMolecular neurobiology2025
MGST1 Inhibits Sevoflurane-Induced Ferroptosis and Activates the Wnt Pathway in HT22 Cells.
Article in Molecular neurobiology, 2025. 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.
- DDIT4 silencing attenuates sevoflurane-induced ferroptosis via the mTOR pathway in neuronal cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Chronic Low-Dose Unsymmetrical Dimethylhydrazine Exposure in Rats: Multiorgan Mechanisms and Biomarker Identification.Journal of applied toxicology : JAT · 2026Article
- Role and mechanism of LINC00662 via targeting let-7 g-5p in sevoflurane-induced cognitive impairment in rats.BMC anesthesiology · 2026Article
- MGST1 drives lymph node metastasis in papillary thyroid carcinoma via mitochondrial metabolic reprogramming and immune suppression.Frontiers in immunology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
Microsomal glutathione S-transferase 1 (MGST1) regulates ferroptosis in cancers, but its engagement in anesthesia-induced neuronal ferroptosis is unclear. This study intended to investigate the influence of MGST1 on ferroptosis in sevoflurane (Sev)-treated HT22 cells. Cells were treated with 1%, 2%, and 4% Sev. HT22 cells were transfected with MGST1 overexpression or negative control plasmids, followed by 4% Sev treatment. Cell viability, oxidative stress markers, iron levels, ferroptosis-related proteins, Wnt pathway, and MGST1 gene expression and protein level were detected. Sev enhanced ferroptosis and reduced MGST1 expression in HT22 cells in a concentration-dependent manner. MGST1 enhanced viability in Sev-treated HT22 cells (P < 0.05). MGST1 reduced reactive oxygen species (ROS) level (P < 0.001) and malondialdehyde (MDA) (P < 0.01), but increased superoxide dismutase (SOD) activity (P < 0.05), indicating that MGST1 inhibited oxidative stress in Sev-treated HT22 cells. MGST1 also reduced Fe
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