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二氢愈创木酸减轻细颗粒物诱导的皮肤亚细胞功能障碍。

Diphlorethohydroxycarmalol Attenuates Fine Particulate Matter-Induced Subcellular Skin Dysfunction.

机构信息

School of Medicine, Jeju National University, Jeju 63243, Korea.

Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 63243, Korea.

出版信息

Mar Drugs. 2019 Feb 1;17(2):95. doi: 10.3390/md17020095.

Abstract

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.

摘要

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。

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