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<p>Skin photodamage affects appearance and increases cancer risk, yet existing treatments are inadequate. Our prior data indicate that skin-derived precursors (SKPs) protect against photodamage via exosome-mediated signaling, though the mechanism is unclear. Exosomes are stable stem cell regulators, but SKPs-derived exosomes (SKPs-Exo) are underexplored in photodamage. To assess SKPs-Exo’s therapeutic potential and mechanism in UVB-induced skin damage using mouse and 3D skin models. SKPs-Exo were isolated via ultracentrifugation and characterized by TEM, NTA, and WB. UVB-irradiated mice and 3D skin models received varying SKPs-Exo doses. We evaluated skin damage, apoptosis (TUNEL), oxidative stress (ROS, MDA, GSH, SOD), inflammation (IL-1β, IL-6, TNF-α), and Nrf2, HO-1, BACH1, and NF-κB expression. SKPs-Exo (30–200&#xa0;nm) expressed CD9, CD63, and TSG101. UVB-induced damage, apoptosis, oxidative stress, and inflammation were dose-dependently reduced by SKPs-Exo, which restored antioxidants, suppressed inflammation, and modulated Nrf2/HO-1 and BACH1/NF-κB pathways (<i>P</i> &lt; 0.05 or <i>P</i> &lt; 0.01). SKPs-Exo alleviate UVB-induced skin damage by reducing apoptosis, oxidative stress and inflammation, likely via activating the Nrf2/HO-1 pathway and suppressing the BACH1/NF-κB pathway, providing a potential therapeutic direction for skin photodamage.</p>

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Protective effects of skin-derived precursor cell exosomes against UVB-induced skin photodamage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月28日

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  • Ke Xian,
  • Lumei Liu,
  • Xin Huang,
  • Qian Tang,
  • Jixiang Xu,
  • Zongjunlin Liu

摘要

Skin photodamage affects appearance and increases cancer risk, yet existing treatments are inadequate. Our prior data indicate that skin-derived precursors (SKPs) protect against photodamage via exosome-mediated signaling, though the mechanism is unclear. Exosomes are stable stem cell regulators, but SKPs-derived exosomes (SKPs-Exo) are underexplored in photodamage. To assess SKPs-Exo’s therapeutic potential and mechanism in UVB-induced skin damage using mouse and 3D skin models. SKPs-Exo were isolated via ultracentrifugation and characterized by TEM, NTA, and WB. UVB-irradiated mice and 3D skin models received varying SKPs-Exo doses. We evaluated skin damage, apoptosis (TUNEL), oxidative stress (ROS, MDA, GSH, SOD), inflammation (IL-1β, IL-6, TNF-α), and Nrf2, HO-1, BACH1, and NF-κB expression. SKPs-Exo (30–200 nm) expressed CD9, CD63, and TSG101. UVB-induced damage, apoptosis, oxidative stress, and inflammation were dose-dependently reduced by SKPs-Exo, which restored antioxidants, suppressed inflammation, and modulated Nrf2/HO-1 and BACH1/NF-κB pathways (P < 0.05 or P < 0.01). SKPs-Exo alleviate UVB-induced skin damage by reducing apoptosis, oxidative stress and inflammation, likely via activating the Nrf2/HO-1 pathway and suppressing the BACH1/NF-κB pathway, providing a potential therapeutic direction for skin photodamage.