Abstract
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 μM C3G for 2 h and UVA irradiated at 12 J/cm2. The cells were then incubated with 80 μM C3G for 12 h 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.
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