α-Lipoic acid inhibits sevoflurane-induced neuronal apoptosis through PI3K/Akt signalling pathway

Rong Ma1, Xiang Wang2, Peipei Peng1

  • 1Department of Anesthesiology, The First Affiliated Hospital, Nanjing Medical University (Jiangsu Province Hospital), Nanjing, 210029, China.

Insights

Sevoflurane anesthesia can cause long-term cognitive impairment in young rats by inducing brain cell apoptosis. Alpha-lipoic acid may protect against this neuronal damage and cognitive dysfunction.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Toxicology

Background:

  • General anesthesia with sevoflurane is common in pediatric patients.
  • Concerns exist regarding potential sevoflurane-induced neurotoxicity, particularly in infants and children.
  • General anesthesia may trigger brain cell apoptosis, impacting cognitive function.

Purpose of the Study:

  • To investigate the neuroprotective effects of alpha-lipoic acid against sevoflurane-induced neuronal apoptosis and cognitive impairment.
  • To elucidate the role of the PI3K/Akt signaling pathway in sevoflurane's neurotoxic effects.

Main Methods:

  • Morris water maze test for cognitive function assessment.
  • Western blotting and immunohistochemistry to evaluate neuronal apoptosis and signaling pathways.
  • Animal model using young rats exposed to sevoflurane.

Main Results:

  • Sevoflurane exposure resulted in long-term cognitive impairment in young rats.
  • Neuronal death in the hippocampus, mediated by the PI3K/Akt pathway, was observed.
  • Alpha-lipoic acid administration mitigated sevoflurane-induced cognitive deficits and neuronal apoptosis.

Conclusions:

  • Sevoflurane anesthesia can lead to cognitive dysfunction and neuronal apoptosis in young animals.
  • Alpha-lipoic acid demonstrates potential as a therapeutic agent to prevent sevoflurane-induced neurotoxicity.
  • Targeting the PI3K/Akt pathway and utilizing alpha-lipoic acid may offer a strategy for managing anesthesia-related cognitive impairment.

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