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<p>Skin photoaging, primarily induced by chronic UVB exposure, lacks effective therapeutic options. Schisandrin A (Sch A), a bioactive compound from <i>Schisandra chinensis</i>, has been traditionally used in East Asian medicine for its anti-inflammatory and antioxidant properties. However, the precise mechanisms by which Sch A exerts photoprotective effects against UVB-induced damage remain unclear, warranting further mechanistic exploration. This study aimed to explore the protective effects of Sch A against UVB-induced damage in HaCaT keratinocytes and ICR mice. Sch A improved cell viability, reduced senescence and apoptosis, and enhanced antioxidant defenses by increasing SOD activity and GSH levels while reducing MDA accumulation in mice. Histological analysis showed that Sch A decreased epidermal thickness and preserved dermal collagen. Molecular assays revealed that Sch A activated AMPK and Nrf2 signaling, promoted autophagy, reduced oxidative stress, and inhibited MMP expression. These findings suggest that Sch A alleviates photoaging by modulating oxidative stress, apoptosis, and autophagy via the AMPK/Nrf2 pathways, offering a promising strategy for skin protection.</p> Graphical abstract <p></p>

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Schisandrin A alleviates UVB-induced photoaging via AMPK/Nrf2-mediated antioxidant and autophagy pathways

  • 期刊论文

  • 发表日期：

    2026年3月9日

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  • Shuangling Wang,
  • Kexin Liu,
  • Meihao Zhang,
  • Shiqi Wang,
  • Zhengyi Li,
  • Wenyue Zhuang

摘要

Skin photoaging, primarily induced by chronic UVB exposure, lacks effective therapeutic options. Schisandrin A (Sch A), a bioactive compound from Schisandra chinensis, has been traditionally used in East Asian medicine for its anti-inflammatory and antioxidant properties. However, the precise mechanisms by which Sch A exerts photoprotective effects against UVB-induced damage remain unclear, warranting further mechanistic exploration. This study aimed to explore the protective effects of Sch A against UVB-induced damage in HaCaT keratinocytes and ICR mice. Sch A improved cell viability, reduced senescence and apoptosis, and enhanced antioxidant defenses by increasing SOD activity and GSH levels while reducing MDA accumulation in mice. Histological analysis showed that Sch A decreased epidermal thickness and preserved dermal collagen. Molecular assays revealed that Sch A activated AMPK and Nrf2 signaling, promoted autophagy, reduced oxidative stress, and inhibited MMP expression. These findings suggest that Sch A alleviates photoaging by modulating oxidative stress, apoptosis, and autophagy via the AMPK/Nrf2 pathways, offering a promising strategy for skin protection.

Graphical abstract