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MicroRNA-96 is responsible for sevoflurane-induced cognitive dysfunction in neonatal rats via inhibiting IGF1R

Chang Xu1, Jiao-Jiao Niu1, Jun-Fei Zhou1

  • 1Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.

Brain Research Bulletin
|September 16, 2018
PubMed

Insights

Sevoflurane anesthesia in neonatal rats increases miR-96, which impairs learning and memory by downregulating IGF1R, leading to cognitive dysfunction. This study identifies miR-96 as a key mediator in sevoflurane-induced cognitive deficits.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Anesthesiology

Background:

  • Sevoflurane is a volatile anesthetic with potential neurotoxic effects.
  • Neonatal exposure to sevoflurane may lead to cognitive deficits and abnormal behaviors.
  • MicroRNAs (miRNAs) play crucial roles in regulating gene expression and neuronal function.

Purpose of the Study:

  • To investigate the relationship between sevoflurane exposure and miR-96 expression in neonatal rats.
  • To determine if miR-96 mediates sevoflurane-induced cognitive dysfunction by targeting IGF1R.
  • To elucidate the molecular mechanisms underlying sevoflurane's impact on learning and memory.

Main Methods:

  • Administered varying concentrations of sevoflurane (1%, 2%, 4%) to neonatal rats.
  • Utilized miR-96 mimics and inhibitors to study its regulatory role.
  • Verified miR-96 targeting of IGF1R using luciferase assays.
  • Assessed hippocampal neuron apoptosis and cognitive function (Morris water maze, step-down test).

Main Results:

  • A positive correlation was found between sevoflurane concentration and miR-96 levels.
  • miR-96 was confirmed to negatively target IGF1R.
  • Higher sevoflurane concentrations (4%) significantly increased miR-96, decreased IGF1R and Bcl-2, and elevated Bax and caspase-3, leading to apoptosis and impaired learning/memory.
  • miR-96 mimic exacerbated sevoflurane's negative effects on neurons and cognition.

Conclusions:

  • miR-96 plays a critical role in sevoflurane anesthesia-induced cognitive dysfunction in neonatal rats.
  • Sevoflurane-induced cognitive deficits are mediated through the downregulation of IGF1R by miR-96.
  • Targeting the miR-96/IGF1R pathway may offer therapeutic strategies for preventing sevoflurane neurotoxicity.
Keywords:
ApoptosisCognitive dysfunctionHippocampal neuronIGF1RMicroRNA-96Sevoflurane

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