Zhang Xing-Jie, Yang Peng-Yun, Ding Ling, Wang Jun, Li Xiao-Li, Xiao Wei-Lie
Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Characteristic Plant Extraction Laboratory, Yunnan Key Laboratory of Research and Development for Natural Products, State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, School of Pharmacy and School of Chemical Science and Technology, Yunnan University, Kunming 650500, Yunnan, China.
Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Characteristic Plant Extraction Laboratory, Yunnan Key Laboratory of Research and Development for Natural Products, State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, School of Pharmacy and School of Chemical Science and Technology, Yunnan University, Kunming 650500, Yunnan, China.
Toxicol Appl Pharmacol. 2025 Apr;497:117262. doi: 10.1016/j.taap.2025.117262. Epub 2025 Feb 8.
Photodamage, a type of skin inflammation caused by excessive exposure to solar radiation, leads to skin redness, inflammation, and even the development of skin cancer, posing a severe threat to individuals living at high altitudes. UVB radiation is considered the primary factor contributing to photodamage. It stimulates macrophages within the epidermis, triggers inflammasome activation, and increases the inflammatory cytokine interleukin-1β (IL-1β) production. This study examined the protective effects of the compound isolicoflavonol (ILF) and its mechanism against UVB-induced photodamage. We irradiated UVB to create a photodamage model in mice and macrophages. Next, we assessed ILF's ability to protect the skin and cells from UVB photodamage and its inhibitory effects on UVB-mediated NLRP3 inflammasome. Our findings indicated that ILF reduced UVB-induced skin injury and inflammation in mouse skin, decreased cell death, NLRP3 inflammasome activation, ROS production, and mitochondrial dysfunction. These results suggest that ILF may be a potent agent for protecting the skin against UVB-induced photodamage.
光损伤是一种由于过度暴露于太阳辐射而引起的皮肤炎症，会导致皮肤发红、炎症，甚至引发皮肤癌，对生活在高海拔地区的人构成严重威胁。紫外线B（UVB）辐射被认为是导致光损伤的主要因素。它刺激表皮内的巨噬细胞，触发炎性小体激活，并增加炎性细胞因子白细胞介素-1β（IL-1β）的产生。本研究考察了化合物异甘草素（ILF）对UVB诱导的光损伤的保护作用及其机制。我们用UVB照射以建立小鼠和巨噬细胞的光损伤模型。接下来，我们评估了ILF保护皮肤和细胞免受UVB光损伤的能力及其对UVB介导的NLRP3炎性小体的抑制作用。我们的研究结果表明，ILF减轻了UVB诱导的小鼠皮肤损伤和炎症，减少了细胞死亡、NLRP3炎性小体激活、活性氧生成和线粒体功能障碍。这些结果表明，ILF可能是一种有效的保护皮肤免受UVB诱导的光损伤的药物。
