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Rapamycin Attenuates H2O2-Induced Oxidative Stress-Related Senescence in Human Skin Fibroblasts

Yuyang Tang1, Sen Yang2, Zhen Qiu1

  • 1School of Stomatology, Zunyi Medical University, Zunyi, China.

Tissue Engineering and Regenerative Medicine
|August 2, 2024
PubMed
Abstract

Insights

Rapamycin protects human skin fibroblasts from oxidative stress and aging by reducing cellular damage and enhancing autophagy. This study reveals rapamycin

Area of Science:

  • Dermatology and aging research
  • Cellular senescence mechanisms
  • Pharmacological interventions for skin health

Background:

  • Oxidative stress is a key driver of skin aging.
  • Rapamycin's anti-aging properties are known, but its effect on oxidative skin cell senescence requires clarification.

Purpose of the Study:

  • To investigate rapamycin's impact on oxidative stress-induced skin cell senescence.
  • To elucidate the underlying molecular mechanisms of rapamycin's action.

Main Methods:

  • Established a hydrogen peroxide (H2O2)-induced oxidative senescence model in human skin fibroblasts (HSFs).
  • Assessed cell proliferation, migration, senescence markers (SA-β-gal, P53, MMP-1, COL1A-1), oxidative stress indicators (SOD, HO-1, ROS, MDA), and autophagy pathway activation via western blotting and qPCR.

Main Results:

  • Rapamycin treatment (0.1 nmol/L for 48h) improved HSF proliferation and migration.
  • It reduced senescence markers and oxidative damage (lower P53, MMP-1, ROS, MDA; higher COL1A-1, SOD, HO-1).
  • Rapamycin significantly upregulated autophagy-related genes and proteins, indicating pathway activation.

Conclusions:

  • Rapamycin effectively protects human skin fibroblasts against H2O2-induced oxidative damage.
  • The protective mechanism involves reducing intracellular peroxidation and activating the autophagy pathway.
  • Rapamycin shows potential for preventing skin aging and mitigating oxidative stress effects.
Keywords:
AutophagyHuman skin fibroblastsOxidative stressRapamycinSenescence

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