School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea.
Aging Research Center, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea.
Environ Toxicol Pharmacol. 2013 Sep;36(2):680-688. doi: 10.1016/j.etap.2013.06.010. Epub 2013 Jun 28.
Exposure of human skin to excessive ultraviolet B (UVB) radiation induces pathophysiological processes via the generation of reactive oxygen species (ROS) in skin cells, such as keratinocytes. This study investigated the ability of diphlorethohydroxycarmalol (DPHC) to protect human keratinocytes (HaCaT) against UVB-induced cell damage. DPHC restored cell viability that was reduced by UVB light. DPHC had an absorption maximum close to the UVB spectrum and decreased UVB-induced intracellular ROS levels, increased levels of reduced glutathione, activated superoxide dismutase and catalase. DPHC also decreased UVB-mediated damage to cellular components, including lipids, proteins, DNA, and attenuated UVB-induced apoptosis. These results suggest that DPHC safeguards human keratinocytes against UVB-induced cell damage by absorbing UVB ray, scavenging ROS and enhancing antioxidant system.
人体皮肤暴露在过量的紫外线 B（UVB）辐射下，会在皮肤细胞（如角质细胞）中产生活性氧（ROS），从而引发病理生理过程。本研究探讨了二苯并呋喃并[1,2-b]色醇（DPHC）保护人角质细胞（HaCaT）免受 UVB 诱导的细胞损伤的能力。DPHC 恢复了被 UVB 光降低的细胞活力。DPHC 的吸收最大值接近 UVB 光谱，并降低了 UVB 诱导的细胞内 ROS 水平，增加了还原型谷胱甘肽的水平，激活了超氧化物歧化酶和过氧化氢酶。DPHC 还减少了 UVB 介导的对包括脂质、蛋白质、DNA 在内的细胞成分的损伤，并减弱了 UVB 诱导的细胞凋亡。这些结果表明，DPHC 通过吸收 UVB 射线、清除 ROS 和增强抗氧化系统来保护人角质细胞免受 UVB 诱导的细胞损伤。
