Department of Dermatology, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China.
Department of Food Science and Engineering, Jinan University, Guangzhou, Guangdong, China.
Photodermatol Photoimmunol Photomed. 2018 Jul;34(4):224-231. doi: 10.1111/phpp.12374. Epub 2018 Jan 25.
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.
Primary HDFs were pretreated with 80 μmol/L C3G for 2 hours and UVA irradiated at 12 J/cm . 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.
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.
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.
背景/目的：紫外线 A（UVA）辐射可引起光老化和皮肤癌，但预防或治疗 UVA 诱导的皮肤损伤的方法仍需进一步研究。本研究旨在探讨矢车菊素-3-O-葡萄糖苷（C3G），一种花青素单体，对人原代真皮成纤维细胞（HDF）中 UVA 诱导损伤的影响，并确定该化合物发挥保护作用的潜在机制。
用 80 μmol/L C3G 预处理原代 HDF 2 小时，然后用 12 J/cm 的 UVA 辐射。照射后，细胞再用 80 μmol/L C3G 孵育 12 小时。将 HDF 随机分为对照组、UVA 处理组、C3G 组和 UVA 处理加 C3G 预处理组。
C3G 增加了原代 HDF 的细胞活力，降低了 UVA 诱导的 ROS 产生和细胞凋亡率。与 UVA 组相比，UVA 加 C3G 预处理组的 Bcl-2 表达和 Bcl-2/Bax 比值增加，caspase-3 切割和 p-P38 水平降低，ERK 磷酸化增加；p-JNK 水平无显著变化。
C3G 减轻了 UVA 诱导的 HDF 氧化损伤和细胞凋亡，这可能与 p-P38 下调、ERK 蛋白磷酸化上调有关。
