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Background/Purpose: Ultraviolet (UV) A (315‐400 nm) is the UV light that most frequently reaches the Earth's surface and can penetrate the epidermis through to the dermis, causing various issues, including skin aging and skin cancer. The results of our previous studies have shown that the flavonoid monomer cyanidin‐3‐o‐glucoside (C3G) can effectively inhibit primary human dermal fibroblast (HDF) oxidative damage and apoptosis caused by UVA radiation. Many flavonoids can regulate the level of autophagy. However, whether C3G inhibits UVA‐induced oxidative damage to primary HDFs by regulating autophagy levels remains unclear. Methods and Results: In this study, we used different doses (0‐12 J/cm2) of UVA to irradiate cells and showed that the expression levels of autophagy‐related gene 5 (Atg5) and microtubule‐associated protein 1 light chain 3 (LC3)‐II in primary HDFs first increased and then decreased. The expression of Atg5 and LC3‐II was significantly decreased under 12 J/cm2 (light‐damage model). C3G increased the levels of Atg5 and LC3‐II. Primary HDFs were pretreated with C3G, followed by treatment with the autophagy inhibitor 3‐methyladenine (3‐MA) after 12 J/cm2 UVA irradiation. The inhibitory effects of C3G on morphological changes, oxidative damage, and apoptosis in primary HDFs induced by UVA were significantly decreased. Conclusion: C3G can inhibit UVA‐induced damage to primary HDFs by inducing autophagy. These results provide a theoretical basis for the application of natural compounds to resist light damage to the skin in the future. [ABSTRACT FROM AUTHOR]

Summary: Background/purpose: Ultraviolet‐A (UVA) radiation can induce photoaging and skin cancer, but means to prevent or treat UVA‐induced skin damage require further study. We investigated the effects of cyanidin‐3‐o‐glucoside (C3G), a monomer of anthocyanin, on UVA‐induced damage in primary human dermal fibroblasts (HDFs), and we identify possible mechanisms underlying the protective effects of this compound. Methods: Primary HDFs were pretreated with 80 μmol/L C3G for 2 hours and UVA irradiated at 12 J/cm2. The cells were then incubated with 80 μmol/L C3G for 12 hours after irradiation. HDFs were randomly divided into control, UVA treatment, C3G, and UVA treatment plus C3G pretreatment groups. Results: C3G increased the cell viability of primary HDFs and decreased UVA‐induced ROS production and apoptosis rate. Compared to the UVA group, the UVA plus pretreatment with C3G group displayed increased Bcl‐2 expression and Bcl‐2/Bax ratio, decreased cleaved caspase‐3 and p‐P38 levels, and increased ERK phosphorylation; no significant effect on p‐JNK levels was observed. Conclusion: C3G reduced UVA‐induced HDF oxidative damage and apoptosis, likely be related to the down‐regulation of p‐P38, up‐regulation of ERK protein phosphorylation. [ABSTRACT FROM AUTHOR]