School of Medicine, Jeju National University, Jeju 63243, Korea.
Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 63243, Korea.
Mar Drugs. 2019 Feb 1;17(2):95. doi: 10.3390/md17020095.
The skin, the largest organ in humans, is exposed to major sources of outdoor air pollution, such as fine particulate matter with a diameter ≤ 2.5 µm (PM). Diphlorethohydroxycarmalol (DPHC), a marine-based compound, possesses multiple activities including antioxidant effects. In the present study, we evaluated the protective effect of DPHC on PM-induced skin cell damage and elucidated the underlying mechanisms in vitro and in vivo. The results showed that DPHC blocked PM-induced reactive oxygen species generation in human keratinocytes. In addition, DPHC protected cells against PM-induced DNA damage, endoplasmic reticulum stress, and autophagy. HR-1 hairless mice exposed to PM showed lipid peroxidation, protein carbonylation, and increased epidermal height, which were inhibited by DPHC. Moreover, PM induced apoptosis and mitogen-activated protein kinase (MAPK) protein expression; however, these changes were attenuated by DPHC MAPK inhibitors were used to elucidate the molecular mechanisms underlying these actions, and the results demonstrated that MAPK signaling pathway may play a key role in PM-induced skin damage.
皮肤是人体最大的器官，它暴露于大气污染的主要来源，如直径≤2.5μm 的细颗粒物（PM）。二苯并对二氢吡喃醇（DPHC）是一种海洋来源的化合物，具有多种活性，包括抗氧化作用。在本研究中，我们评估了 DPHC 对 PM 诱导的皮肤细胞损伤的保护作用，并在体外和体内阐明了其潜在机制。结果表明，DPHC 阻断了 PM 诱导的人角质形成细胞中活性氧的产生。此外，DPHC 可保护细胞免受 PM 诱导的 DNA 损伤、内质网应激和自噬。暴露于 PM 的 HR-1 无毛小鼠表现出脂质过氧化、蛋白质羰基化和表皮高度增加，而 DPHC 抑制了这些变化。此外，PM 诱导细胞凋亡和丝裂原激活蛋白激酶（MAPK）蛋白表达；然而，DPHC 减弱了这些变化。使用 MAPK 抑制剂阐明了这些作用的分子机制，结果表明 MAPK 信号通路可能在 PM 诱导的皮肤损伤中发挥关键作用。
