Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Madecassoside attenuated UVB irradiation-induced skin ferroptosis by targeting POR.
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Liu Lingxia, Niu Pengxiang, Xiao Bo, Ma Haotian, Cui Yating, Ma Xizhi, Pei Xinyun, Liu Qian, Shan Ningyu, Xu Tong, Xu Haixu, Zhou Xiaotao, Li Xichuan
Аннотация
BACKGROUND: UVB exposure induces oxidative damage and accelerates skin photoaging. Madecassoside (MA), a triterpenoid saponin from Centella asiatica (L.) Urban, has antioxidant and anti-inflammatory properties, but its role in ferroptosis remains unclear.
PURPOSE: This study aims to investigate the effects of MA against UVB-induced ferroptosis and elucidate its underlying mechanisms.
STUDY DESIGN: Skin cells and a UVB-irradiated mouse model were established to assess the effects of MA on UVB-induced ferroptosis and skin damage.
METHODS: Skin cells and a UVB-irradiated mouse model were used to assess MA's effects on ferroptosis. ROS, lipid ROS, mitochondrial membrane potential and antioxidant enzyme activity were measured. Protein and gene expression of ferroptosis markers were analyzed via Western blot and qPCR. Transmission electron microscopy (TEM) examined mitochondrial morphology.
RESULTS: UVB irradiation induced ferroptosis in human skin cells, characterized by lipid peroxidation, ROS accumulation, mitochondrial dysfunction, and antioxidant depletion. MA treatment significantly inhibited ferroptosis and restored redox balance. In mice, topical MA application enhanced collagen deposition, reduced epidermal thickening, and alleviated ferroptosis. Mechanistically, MA bound to and downregulated the NADPH-cytochrome P450 reductase (POR), a key regulator of ferroptosis and POR overexpression negated MA's protective effects.
CONCLUSION: This study demonstrates that MA protects against UVB-induced ferroptosis via POR inhibition, highlighting its potential for therapeutic and cosmetic applications in preventing ferroptosis.
PURPOSE: This study aims to investigate the effects of MA against UVB-induced ferroptosis and elucidate its underlying mechanisms.
STUDY DESIGN: Skin cells and a UVB-irradiated mouse model were established to assess the effects of MA on UVB-induced ferroptosis and skin damage.
METHODS: Skin cells and a UVB-irradiated mouse model were used to assess MA's effects on ferroptosis. ROS, lipid ROS, mitochondrial membrane potential and antioxidant enzyme activity were measured. Protein and gene expression of ferroptosis markers were analyzed via Western blot and qPCR. Transmission electron microscopy (TEM) examined mitochondrial morphology.
RESULTS: UVB irradiation induced ferroptosis in human skin cells, characterized by lipid peroxidation, ROS accumulation, mitochondrial dysfunction, and antioxidant depletion. MA treatment significantly inhibited ferroptosis and restored redox balance. In mice, topical MA application enhanced collagen deposition, reduced epidermal thickening, and alleviated ferroptosis. Mechanistically, MA bound to and downregulated the NADPH-cytochrome P450 reductase (POR), a key regulator of ferroptosis and POR overexpression negated MA's protective effects.
CONCLUSION: This study demonstrates that MA protects against UVB-induced ferroptosis via POR inhibition, highlighting its potential for therapeutic and cosmetic applications in preventing ferroptosis.