Schisandrin A alleviates UVB-induced photoaging via AMPK/Nrf2-mediated antioxidant and autophagy pathways.
Abstract
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.
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Research summary
Schisandrin A alleviates UVB-induced photoaging by activating AMPK/Nrf2 signaling pathways to enhance antioxidant defenses and promote autophagy. The study addresses mechanisms related to oxidative stress and cellular aging, which are fundamental to the aging process and longevity.
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