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The effect of Cyanidin‐3‐o‐glucoside on UVA ‐induced damage in human dermal fibroblasts
Author(s) -
Wu Shi,
Hu Yunfeng,
Li Zhen,
Bai Weibin,
Zhao Jiayi,
Huang Cuiqin,
Li Qin,
Fan Chongzhu,
Deng Liehua,
Lu Daxiang
Publication year - 2018
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12374
Subject(s) - photoaging , apoptosis , chemistry , mapk/erk pathway , p38 mitogen activated protein kinases , anthocyanin , phosphorylation , viability assay , antioxidant , andrology , microbiology and biotechnology , biochemistry , biology , medicine , dermatology , food science
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 ( HDF s), and we identify possible mechanisms underlying the protective effects of this compound. Methods Primary HDF s were pretreated with 80 μmol/L C3G for 2 hours and UVA irradiated at 12 J/cm 2 . The cells were then incubated with 80 μmol/L C3G for 12 hours after irradiation. HDF s were randomly divided into control, UVA treatment, C3G, and UVA treatment plus C3G pretreatment groups. Results C3G increased the cell viability of primary HDF s 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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