Home General Physiology and Biophysics 2026 General Physiology and Biophysics Vol.45, No.1, p, 93–105, 2026

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
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General Physiology and Biophysics Vol.45, No.1, p, 93–105, 2026

Title: lncRNA H19 contributes to sevoflurane-induced neuronal death in SH-SY5Y cells via ACSL4-mediated ferroptosis pathway
Author: Lixin Liu, Zhaoping Xue, Yan Liu, Ying Liu
Abstract:  Sevoflurane induces neurotoxicity and cognitive impairment, with long noncoding RNAs (lncRNAs) playing key roles in nervous system diseases. This study explored lncRNA H19’s function in sevoflurane-induced neurotoxicity. SH-SY5Y cell viability and apoptosis were assessed via CCK8 and TUNEL assays. Gene expression was measured by RT-qPCR, while reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and iron levels were quantified. Subcellular fractionation determined H19 localization, and luciferase assays confirmed H19/miR-20a-5p and miR-20a-5p/Acyl-CoA synthetase long chain family member 4 (ACSL4) interactions. Western blot analyzed ACSL4, apoptosis-, and ferroptosis-related proteins. The results showed that sevoflurane reduced viability, promoted apoptosis and ferroptosis, and upregulated H19 and ACSL4. H19 knockdown mitigated neurotoxicity by restoring viability, GSH, solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4), while reducing apoptosis, MDA, ROS, and iron. Mechanistically, H19 sponged miR-20a-5p to elevate ACSL4. Rescue assays showed miR-20a-5p inhibition or ACSL4 overexpression reversed H19 silencing’s protective effects. Thus, H19 depletion alleviates sevoflurane-induced neuronal damage via the miR-20a-5p/ACSL4 axis, suggesting a potential therapeutic target.
Keywords: Long noncoding RNA H19 — Ferroptosis — Sevoflurane — ACSL4
Year: 2026, Volume: 45, Issue: 1 Page From: 93, Page To: 105
doi:10.4149/gpb_2025025
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