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Peer-reviewedCC BY-NC-NDJournal of biochemical and molecular toxicology

Protective Role of miR-432-5p Against Propofol-Induced Neurotoxicity Through Regulation of ITK in SH-SY5Y Cells.

  • Aijing Shi1
  • Changke Li1
  1. 1Anesthesiology Department, Aoyang Hospital Affiliated to Jiangsu University, Suzhou, China.
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Abstract

The widespread use of propofol in pediatric anesthesia raises significant concerns regarding its potential neurodevelopmental toxicity and long-term cognitive impairment in children. To explore the protective role of miR-432-5p against propofol-induced neurotoxicity and clarify its underlying mechanisms mediated by targeting interleukin-2-inducible T-cell kinase (ITK). An in vitro model of propofol-induced damage was constructed using the SH-SY5Y cell line. Cell survival, the percentage of apoptosis, and the secretion of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) were subsequently quantified. Finally, the direct interaction between miR-432-5p and its target, ITK, was verified through dual-luciferase reporter assays. miR-432-5p was markedly downregulated following propofol exposure. In vitro, miR-432-5p overexpression improved cell viability, reduced apoptosis, and suppressed pro-inflammatory cytokine release. ITK was validated as a direct downstream target of miR-432-5p. Furthermore, compensatory overexpression of ITK partially reversed the anti-apoptotic and anti-inflammatory protective phenotypes induced by miR-432-5p. The miR-432-5p/ITK regulatory axis significantly mitigates propofol-induced cellular injury by restraining apoptosis and neuroinflammation. Maintaining miR-432-5p abundance provides a promising theoretical basis and therapeutic target for preventing anesthesia-related cognitive impairment.

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Cite

BibTeXRIS
BibTeX
@article{shi2026protective,
  title = {{Protective Role of miR-432-5p Against Propofol-Induced Neurotoxicity Through Regulation of ITK in SH-SY5Y Cells.}},
  author = {Aijing Shi and Changke Li},
  journal = {Journal of biochemical and molecular toxicology},
  year = {2026},
  month = nov,
  doi = {10.1002/jbt.71153},
  url = {https://europepmc.org/article/MED/42967583},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Protective Role of miR-432-5p Against Propofol-Induced Neurotoxicity Through Regulation of ITK in SH-SY5Y Cells.
AU  - Aijing Shi
AU  - Changke Li
PY  - 2026
DA  - 2026/11/01
JO  - Journal of biochemical and molecular toxicology
DO  - 10.1002/jbt.71153
UR  - https://europepmc.org/article/MED/42967583
AB  - The widespread use of propofol in pediatric anesthesia raises significant concerns regarding its potential neurodevelopmental toxicity and long-term cognitive impairment in children. To explore the protective role of miR-432-5p against propofol-induced neurotoxicity and clarify its underlying mechanisms mediated by targeting interleukin-2-inducible T-cell kinase (ITK). An in vitro model of propofol-induced damage was constructed using the SH-SY5Y cell line. Cell survival, the percentage of apoptosis, and the secretion of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) were subsequently quantified. Finally, the direct interaction between miR-432-5p and its target, ITK, was verified through dual-luciferase reporter assays. miR-432-5p was markedly downregulated following propofol exposure. In vitro, miR-432-5p overexpression improved cell viability, reduced apoptosis, and suppressed pro-inflammatory cytokine release. ITK was validated as a direct downstream target of miR-432-5p. Furthermore, compensatory overexpression of ITK partially reversed the anti-apoptotic and anti-inflammatory protective phenotypes induced by miR-432-5p. The miR-432-5p/ITK regulatory axis significantly mitigates propofol-induced cellular injury by restraining apoptosis and neuroinflammation. Maintaining miR-432-5p abundance provides a promising theoretical basis and therapeutic target for preventing anesthesia-related cognitive impairment.
SN  - 1095-6670
SN  - 1099-0461
ER  -