Atractylodin mitigates UVB radiation-induced oxidative stress and photoaging responses by enhancing NrF2 signaling in human epidermal keratinocytes.

This study explores the protective role of Atractylodin (ATN) on ultraviolet-B (UVB) radiation-exposed oxidative damage and photoaging responses in human epidermal keratinocytes (HaCaT). In vitro, experiments involved subjecting HaCaT cells to UVB radiation (50 mJ/cm) for a 24 h incubation period, leading to cell death, increased reactive oxygen species (ROS), and DNA damaged lesion (8-Oxo Gunosine). ATN treatment effectively mitigated cell toxicity, ROS generation, and 8-Oxo Gunosine in UVB-exposed HaCaT cells. Furthermore, ATN demonstrated its ability to counteract UVB radiation-exposed oxidative stress by inhibiting the activation of phosphorylated-extracellular signal-regulated kinase-1 (Erk-1), phosphorylated-c-Jun N-terminal kinase (p-Jnk), and phosphorylated p38 Mitogen-Activated Protein Kinase (p-p38) in HaCaT cells. Nuclear factor erythroid 2-related factor 2 (NrF2), recognized for its antioxidant properties, emerged as a key player in protecting against oxidative damage. ATN was observed to inhibit the depletion of NrF2 expression, thereby preventing the depletion of superoxide dismutase (SOD), and glutathione (GSH) in UVB-exposed HaCaT cells. Additionally, ATN inhibited activator protein-1 (AP-1) and matrix metalloproteinases such as MMP-1 and MMP-9 in UVB-exposed HaCaT cells. In conclusion, our findings highlight that ATN effectively prevents UVB-exposed skin oxidative damage and photoaging by modulating NrF2 expression.