Tan Hongyan, Ren Honghong, Chai Jiayi, Zhai Changzhen, Li Tao, Zhou Xinyang, Lee Jungjoon, Li Xiaomin, Zhao Yuqing
Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, College of Pharmacy, Yanbian University, Yanji, Jilin Province 133002, China.
Perfect (Guangdong) Co., Ltd., Guangdon, 528400, China.
Food Res Int. 2024 Dec;198:115379. doi: 10.1016/j.foodres.2024.115379. Epub 2024 Nov 20.
Ultraviolet (UV) B irradiation is closely related to skin aging and skin damage. Here, we report the photoprotective mechanism of action of ginseng berry rare saponins (GFRS) on UVB-induced damage to human keratinocytes and mouse skin. Several UVB irradiation-induced cytotoxicity and oxidative stress responses were assessed. GFRS preconditioning significantly improved HaCaT cell survival and reduced the levels of the DNA damage markers histone H2AX and cyclobutane pyrimidine dimer. Under oxidative stress, GFRS could reduce the transformation and loss of the mitochondrial membrane potential to the monomer form; effectively clear the expression of lipid reactive oxygen species, malondialdehyde, and other peroxides, and restore total superoxide dismutase, glutathione peroxidase, and catalase levels. The occurrence of ferroptosis after UVB induction was also studied. Erastin exacerbated the induced cellular iron overload, whereas GFRS and Fer-1 reversed this response to varying degrees. Mechanistically, GFRS activated the Nrf2/HO-1/GPX4 pathway and inhibited the phenomenon of ferroptosis in cells. Our findings were confirmed using a mouse model of UV induced skin injury. GFRS not only mitigated lipid peroxides and iron overload in tissues but also prevented skin barrier damage and collagen loss. Therefore, GFRS shows potential as a novel functional product as it protects the skin from UVB light-induced damage.
紫外线B（UVB）照射与皮肤衰老和皮肤损伤密切相关。在此，我们报告人参果稀有皂苷（GFRS）对UVB诱导的人角质形成细胞和小鼠皮肤损伤的光保护作用机制。评估了几种UVB照射诱导的细胞毒性和氧化应激反应。GFRS预处理显著提高了HaCaT细胞的存活率，并降低了DNA损伤标志物组蛋白H2AX和环丁烷嘧啶二聚体的水平。在氧化应激下，GFRS可以减少线粒体膜电位向单体形式的转变和丧失；有效清除脂质活性氧、丙二醛等过氧化物的表达，并恢复总超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶水平。还研究了UVB诱导后铁死亡的发生情况。埃拉斯汀加剧了诱导的细胞铁过载，而GFRS和Fer-1不同程度地逆转了这种反应。从机制上讲，GFRS激活了Nrf2/HO-1/GPX4通路并抑制了细胞中的铁死亡现象。我们的研究结果在UV诱导的皮肤损伤小鼠模型中得到了证实。GFRS不仅减轻了组织中的脂质过氧化物和铁过载，还防止了皮肤屏障损伤和胶原蛋白流失。因此，GFRS作为一种新型功能性产品具有潜力，因为它可以保护皮肤免受UVB光诱导的损伤。
