Home General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.3, p 285–295, 2023

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

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General Physiology and Biophysics Vol.42, No.3, p 285–295, 2023

Title: Knockdown of lncRNA NKILA suppresses sevoflurane-induced neuronal cell injury partially by targeting miR-205-5p/ELAVL1 axis
Author: Yilong Zhang, Changbai Chen
Abstract: Sevoflurane (Sev) is a wildly used volatile anesthetic agent that induces neurotoxicity. Long non-coding RNAs (lncRNAs) have been demonstrated to be involved in Sev-induced neuronal injury. Here, we investigated the role of NF-kappaB-interacting lncRNA (NKILA) in Sev-treated human cortical neurons (HCN). From RT-qPCR, Sev dose-dependently increased HCN NKILA transcript expression. Neurotoxicity of Sev was detected using MTT, flow cytometry, Western blotting, and inflammatory mediator assays. Consequently, Sev reduced HCN viability and levels of Bcl-2, SOD, and GSH in HCN, and promoted HCN apoptosis rate and levels of cleaved-caspase-3, Bax, MDA, TNF-α, IL-6, and IL-1β. Silencing NKILA suppressed Sev-induced above effects. DIANA and starbase databases predicted the potential target relationship between miR-205-5p and NKILA or embryonic lethal abnormal vision-like 1 (ELAVL1); dual-luciferase and RIP confirmed these interactions. NKILA could increase ELAVL1 expression by regulating miR-205-5p. miR-205-5p overexpression and ELAVL1 knockdown could mimic effects of NKILA silencing in Sev-induced HCN. Deleting miR-205-5p and restoring ELAVL1 respectively abolished the neuroprotective effect of NKILA knockdown and miR-205-5p upregulation under Sev anesthesia. In conclusion, Sev induced neuronal cell apoptosis, inflammatory response and oxidative stress through NKILA/miR-205-5p/ELAVL1 axis and caspase-3 and Bax/Bcl-2 pathway. Inhibiting NKILA might be a potential therapeutic strategy for Sev neurotoxicity.
Keywords: Sevoflurane — Neuron — NKILA — miR-205-5p — ELAVL1
Published online: 02-May-2023
Year: 2023, Volume: 42, Issue: 3 Page From: 285, Page To: 295
doi:10.4149/gpb_2023007


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