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RE-1 silencing transcription factor alleviates the growth-suppressive effects of propofol on mouse neuronal cells

Chunliang Liu1, Sheng Peng, Qingyang Li

  • 1aDepartment of Anesthesiology, Seventh People's Hospital of Shanghai University of TCM bDepartment of Anesthesiology, Shanghai Songjiang District Central Hospital, Shanghai City, PR China.

Neuroreport
|September 11, 2019
PubMed
Abstract

Insights

Propofol inhibits neuronal cell proliferation and promotes apoptosis. The RE-1 silencing transcription factor and autophagy pathway are involved in propofol

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Propofol is a widely used anesthetic.
  • Propofol influences neurogenesis and neurodegeneration through autophagy and calcium homeostasis.
  • The precise molecular mechanisms remain unclear.

Purpose of the Study:

  • To investigate the effects of propofol on mouse neuronal cells (HT-22).
  • To elucidate the molecular pathways mediating propofol's actions on neuronal cells.

Main Methods:

  • Cell Counting Kit-8 assays for proliferation.
  • Flow cytometry for apoptosis analysis.
  • Quantitative real-time PCR and Western blot for gene and protein expression analysis.

Main Results:

  • Propofol inhibited neuronal cell proliferation and induced apoptosis.
  • Overexpression of RE-1 silencing transcription factor (REST) reversed propofol's effects.
  • Autophagy inhibition using 3-methyladenine also mitigated propofol's impact.
  • REST overexpression increased brain-derived neurotrophic factor (BDNF) expression.

Conclusions:

  • Propofol negatively impacts neuronal cell proliferation and survival.
  • The REST and autophagy pathways play a significant role in propofol's neurotoxic effects.
  • REST may mediate propofol's influence on BDNF expression.

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