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<p> This study aimed to unravel the underlying mechanism of dexmedetomidine (Dex) in mitigating anesthesia-induced neurotoxicity secondary to sevoflurane (Sev) exposure. Human Neuroblastoma Cells (SK-N-SH) were assessed for cytotoxicity by quantifying cell viability via CCK-8 assay, lactate dehydrogenase (LDH) release using an LDH kit, inflammatory cytokines factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) levels via ELISA kits, reactive oxygen species (ROS) production with an ROS assay kit, and apoptosis by flow cytometry, respectively. Cellular expression of miR-34a and SIRT1 was measured using RT-qPCR. Dual-luciferase assays mechanistically validated the functional binding of miR-34a to the SIRT1 3’UTR. Sev concentration-dependently reduced cell viability and promoted LDH release, ROS production, cytokines generation, and apoptosis, whereas Dex attenuated Sev-induced neurotoxicity. Sev significantly elevates cellular expression levels of miR-34a, which subsequently binds to and functionally suppresses SIRT1 through post-transcriptional regulatory mechanisms. Dex reduced Sev-induced miR-34a upregulation and increased SIRT1 expression, thereby enhancing SK-N-SH cell viability while decreasing LDH release, ROS production, cytokine generation, and apoptosis. These findings indicated that Dex attenuated Sev-induced neurotoxicity by downregulating miR-34a expression to subsequently upregulate SIRT1 levels.</p>

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The protective role of dexmedetomidine against anaesthetics-induced neurotoxicity through downregulating miR-34a

  • 期刊论文

  • 发表日期：

    2025年10月14日

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  • Ninghao Chen,
  • Bo Wang,
  • Zhenbin Zhan,
  • Hai Chen,
  • Jinguang Chen,
  • Ye Cai

摘要

This study aimed to unravel the underlying mechanism of dexmedetomidine (Dex) in mitigating anesthesia-induced neurotoxicity secondary to sevoflurane (Sev) exposure. Human Neuroblastoma Cells (SK-N-SH) were assessed for cytotoxicity by quantifying cell viability via CCK-8 assay, lactate dehydrogenase (LDH) release using an LDH kit, inflammatory cytokines factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) levels via ELISA kits, reactive oxygen species (ROS) production with an ROS assay kit, and apoptosis by flow cytometry, respectively. Cellular expression of miR-34a and SIRT1 was measured using RT-qPCR. Dual-luciferase assays mechanistically validated the functional binding of miR-34a to the SIRT1 3’UTR. Sev concentration-dependently reduced cell viability and promoted LDH release, ROS production, cytokines generation, and apoptosis, whereas Dex attenuated Sev-induced neurotoxicity. Sev significantly elevates cellular expression levels of miR-34a, which subsequently binds to and functionally suppresses SIRT1 through post-transcriptional regulatory mechanisms. Dex reduced Sev-induced miR-34a upregulation and increased SIRT1 expression, thereby enhancing SK-N-SH cell viability while decreasing LDH release, ROS production, cytokine generation, and apoptosis. These findings indicated that Dex attenuated Sev-induced neurotoxicity by downregulating miR-34a expression to subsequently upregulate SIRT1 levels.