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.
Keywords: apoptosis; cyanidin-3-o-glucoside; human dermal fibroblasts; reactive oxygen species; ultraviolet-A.
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.