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APE1/Ref-1 redox function contributes to inflammatory pain sensitization.

Amira Zaky1, Rabia Bouali-Benazzouz2, Alexandre Favereaux2

  • 1Department of Biochemistry, Faculty of Science, Alexandria University, Moharram Bek, PO Box 21511, Egypt; Bordeaux University, Bordeaux, France; Interdisciplinary Institute for Neuroscience, UMR 5297, CNRS, Bordeaux, France.

Experimental Neurology
|May 18, 2018
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Summary
This summary is machine-generated.

Apurinic/apyrimidinic endonuclease 1 (APE1) expression changes in the central nervous system are linked to inflammatory pain. Inhibiting APE1

Keywords:
APE1/Ref-1InflammationPain sensitizationRedox functionSub-cellular distribution

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Inflammatory pain is a complex condition.
  • Apurinic/apyrimidinic endonuclease 1 (APE1), also known as Redox Factor-1 (Ref-1), is crucial for cellular functions, including oxidative stress regulation.
  • APE1 is expressed in the central nervous system.

Purpose of the Study:

  • To investigate APE1 modulation in an inflammatory pain model.
  • To assess the effects of the APE1 inhibitor E3330 on pain behavior and inflammation.

Main Methods:

  • Complete Freund's adjuvant (CFA) model of inflammatory pain in rats.
  • Analysis of APE1 mRNA and protein expression and subcellular distribution.
  • Administration of E3330, a selective APE1-redox activity inhibitor.
  • Measurement of pain behavior using the von Frey test.
  • Assessment of IL-6 expression.

Main Results:

  • CFA injection altered APE1 expression and subcellular distribution, with reduced overall levels and increased nuclear accumulation.
  • E3330 treatment normalized APE1 mRNA expression and promoted cytosolic accumulation.
  • E3330 reduced IL-6 expression and alleviated inflammatory pain in CFA-treated rats.

Conclusions:

  • Changes in APE1 expression and subcellular distribution are involved in inflammatory pain mechanisms.
  • APE1 redox functions play a role in inflammatory pain.
  • Further research is needed to fully understand APE1's function in inflammatory pain.