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Related Experiment Video

Updated: Oct 25, 2025

Development of an Economical DNA Delivery System by "Acufection" and its Application to Skin Research
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Apremilast ameliorates IL-1α-induced dysfunction in epidermal stem cells.

Yuxi Jia1, Xiangru Chen1, Jing Sun1

  • 1Department of Dermatology, The China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China.

Aging
|August 10, 2021
PubMed
Summary

Apremilast protects epidermal stem cells (ESCs) from IL-1α-induced damage by reducing oxidative stress and inflammation. This occurs through the inhibition of the Myd88/TRAF6/NF-κB signaling pathway, preserving ESC function.

Keywords:
ApremilastESCsIL-1αinflammationoxidative stress

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Area of Science:

  • Dermatology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Epidermal stem cells (ESCs) are crucial for skin barrier repair.
  • External factors like IL-1α can induce oxidative stress and inflammation, impairing ESC self-repair.
  • Apremilast, a phosphodiesterase 4 inhibitor, is approved for psoriasis treatment.

Purpose of the Study:

  • To investigate the protective effects of Apremilast on epidermal stem cells (ESCs) against IL-1α-induced dysfunction.
  • To elucidate the preliminary mechanism underlying Apremilast's protective action.

Main Methods:

  • ESCs were isolated from neonatal mice.
  • Key inflammatory markers (TNF-α, IL-8, IL-12), matrix metalloproteinases (MMP-2, MMP-9), and IL-1R1 were quantified via real-time PCR and ELISA.
  • Mitochondrial reactive oxygen species (ROS) levels were measured using MitoSOX Red assay.
  • Western blot and real-time PCR assessed Myd88, TRAF6, and NF-κB pathway activation (p-NF-κB p65, luciferase activity).
  • ESC capacities were evaluated by measuring integrin β1 and Krt19 gene expression.

Main Results:

  • IL-1α significantly increased TNF-α, IL-8, IL-12, MMP-2, MMP-9, IL-1R1, and ROS levels, which were markedly reduced by Apremilast.
  • Apremilast inhibited the IL-1α-induced activation of the Myd88/TRAF6/NF-κB signaling pathway.
  • Apremilast treatment preserved ESC function, evidenced by elevated integrin β1 and Krt19 expression.

Conclusions:

  • Apremilast demonstrates protective properties against IL-1α-induced epidermal stem cell (ESC) dysfunction.
  • The mechanism involves mitigating oxidative stress and inflammation by inhibiting the Myd88/TRAF6/NF-κB signaling pathway.
  • Apremilast may represent a therapeutic strategy for conditions involving ESC damage due to oxidative stress and inflammation.