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The potential dual effects of sevoflurane on AKT/GSK3β signaling pathway

Lei Zhang, Jie Zhang, Yuanlin Dong

  • 1Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St,, Room 4310, Charlestown, MA 02129-2060, USA. zxie@mgh.harvard.edu.

Medical Gas Research
|March 4, 2014
PubMed
Abstract

Insights

Sevoflurane anesthesia shows a dual effect on the AKT/GSK3β pathway, increasing activation after short exposure and decreasing it after prolonged exposure in both mice and human cells.

Area of Science:

  • Neuroscience
  • Anesthesiology
  • Molecular Biology

Background:

  • Multiple sevoflurane exposures cause neuroinflammation and cognitive deficits in young mice.
  • The AKT/glycogen synthase kinase 3β (GSK3β) signaling pathway is implicated in neurotoxicity.
  • The dual effect of sevoflurane on AKT/GSK3β pathway activation is not well understood.

Purpose of the Study:

  • To investigate the effects of sevoflurane on AKT/GSK3β signaling.
  • To determine if sevoflurane induces a dual effect (increase vs. decrease) on AKT/GSK3β pathway activation.
  • To assess sevoflurane's impact in vivo and in vitro.

Main Methods:

  • Young mice exposed to 3% sevoflurane daily for 1 or 3 days.
  • H4 human neuroglioma cells treated with 4% sevoflurane for 2 or 6 hours.
  • Western blot analysis used to measure phosphorylated AKT (P-AKT) and GSK3β (P-GSK3β).

Main Results:

  • Single-day sevoflurane exposure increased P-AKT and P-GSK3β levels in mice.
  • Three-day sevoflurane exposure decreased P-AKT and P-GSK3β levels in mice.
  • Short-term sevoflurane treatment increased levels in cells, while long-term treatment decreased them.

Conclusions:

  • Sevoflurane may exert dual effects on AKT/GSK3β pathway activation.
  • These findings provide a system for further research into sevoflurane's effects on brain function.

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