Tannic acid prevents UVB-induced skin photoaging by regulating ferroptosis through NRF2/SLC7A11/GPX4 signaling.

BACKGROUND

Photoaging is a significant contributor to accelerated skin aging, primarily driven by ultraviolet B (UVB) radiation exposure, which induces damage to skin tissues. Tannic acid (TA), a high-molecular-weight, water-soluble polyphenolic compound abundant in Galla chinensis and other plant sources, exhibits remarkable antioxidant properties. This study aimed to investigate the effects of TA on UVB-induced skin photoaging and to elucidate the molecular mechanisms underlying.

METHODS

In vitro, TA was applied to UVB-irradiated human skin fibroblast (HSF) cells. we measured cell viability, reactive oxygen species (ROS), markers of cellular senescence, and the activity of antioxidant enzymes. The potential mechanism of TA was explored using RNA sequencing and further verified by Western blotting and administration of ferroptosis inducers. In vivo, we employed a UVB-induced Balb/C mouse model of photoaging to assess epidermal thickness and collagen fiber density. Tissue levels of antioxidant enzymes were also examined, and the expression of mitogen-activated protein kinase (MAPK) and ferroptosis-related protein levels were detected by Western blotting.

RESULTS

TA demonstrated efficacy in mitigating UVB-induced photoaging in fibroblasts. It attenuates oxidative stress damage, inhibited the onset of ferroptosis by modulating MAPK signaling, reduces Fe2+ accumulation, and activated the NRF2/SLC7A11/GPX4 signaling cascade, thereby alleviating photoaging. Furthermore, TA ameliorated UVB-induced epidermal thickening and collagen disruption in mice.

CONCLUSION

This study underscores the protective effects of TA against UVB-induced photoaging in HSF cells and skin tissue. These findings provide a robust theoretical foundation for the development of TA-based natural products intended for anti-photoaging applications.