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Madecassoside attenuated UVB irradiation-induced skin ferroptosis by targeting POR
Lingxia Liu1, Pengxiang Niu1, Bo Xiao2
1Tianjin Key Laboratory of Animal and Plant Resistance, College of Life Sciences, Tianjin Normal University, Tianjin 300387, China.
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.
Insights
Madecassoside (MA) prevents skin damage from UVB exposure by inhibiting ferroptosis, a cell death pathway. MA targets NADPH-cytochrome P450 reductase (POR), offering potential cosmetic and therapeutic benefits against photoaging.
Area of Science:
- Dermatology and molecular biology research.
- Investigating cellular mechanisms of skin aging and damage.
Background:
- UVB radiation causes oxidative stress and skin photoaging.
- Madecassoside (MA), from Centella asiatica, has known antioxidant effects.
- MA's role in ferroptosis, a form of regulated cell death, was previously unknown.
Purpose of the Study:
- To determine if MA protects against UVB-induced ferroptosis.
- To uncover the molecular mechanisms by which MA exerts its protective effects.
Main Methods:
- Utilized human skin cells and a UVB-irradiated mouse model.
- Assessed ferroptosis markers, reactive oxygen species (ROS), lipid ROS, mitochondrial function, and antioxidant enzyme activity.
- Analyzed protein and gene expression of ferroptosis markers and examined mitochondrial morphology via TEM.
Main Results:
- UVB induced ferroptosis in skin cells, marked by increased ROS and mitochondrial dysfunction.
- MA treatment suppressed ferroptosis, restored redox balance, and improved skin condition in mice.
- MA inhibited ferroptosis by downregulating NADPH-cytochrome P450 reductase (POR); POR overexpression counteracted MA's benefits.
Conclusions:
- Madecassoside effectively protects skin against UVB-induced ferroptosis.
- The mechanism involves the inhibition of POR, a key ferroptosis regulator.
- MA shows promise for cosmetic and therapeutic applications in preventing skin damage and aging.
