Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway
Toxicity of particulate matter (PM) towards the epidermis has been well established in many epidemiological studies. It is manifested in cancer, aging, and skin damage. In this study, we aimed to show the mechanism underlying the protective effects of eckol, a phlorotannin isolated from brown seawee...
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MDPI AG
2019-07-01
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author | Ao Xuan Zhen Yu Jae Hyun Mei Jing Piao Pincha Devage Sameera Madushan Fernando Kyoung Ah Kang Mee Jung Ahn Joo Mi Yi Hee Kyoung Kang Young Sang Koh Nam Ho Lee Jin Won Hyun |
author_facet | Ao Xuan Zhen Yu Jae Hyun Mei Jing Piao Pincha Devage Sameera Madushan Fernando Kyoung Ah Kang Mee Jung Ahn Joo Mi Yi Hee Kyoung Kang Young Sang Koh Nam Ho Lee Jin Won Hyun |
author_sort | Ao Xuan Zhen |
collection | DOAJ |
description | Toxicity of particulate matter (PM) towards the epidermis has been well established in many epidemiological studies. It is manifested in cancer, aging, and skin damage. In this study, we aimed to show the mechanism underlying the protective effects of eckol, a phlorotannin isolated from brown seaweed, on human HaCaT keratinocytes against PM<sub>2.5</sub>-induced cell damage. First, to elucidate the underlying mechanism of toxicity of PM<sub>2.5</sub>, we checked the reactive oxygen species (ROS) level, which contributed significantly to cell damage. Experimental data indicate that excessive ROS caused damage to lipids, proteins, and DNA and induced mitochondrial dysfunction. Furthermore, eckol (30 μM) decreased ROS generation, ensuring the stability of molecules, and maintaining a steady mitochondrial state. The western blot analysis showed that PM<sub>2.5</sub> promoted apoptosis-related protein levels and activated MAPK signaling pathway, whereas eckol protected cells from apoptosis by inhibiting MAPK signaling pathway. This was further reinforced by detailed investigations using MAPK inhibitors. Thus, our results demonstrated that inhibition of PM<sub>2.5</sub>-induced cell apoptosis by eckol was through MAPK signaling pathway. In conclusion, eckol could protect skin HaCaT cells from PM<sub>2.5</sub>-induced apoptosis via inhibiting ROS generation. |
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issn | 1660-3397 |
language | English |
last_indexed | 2024-04-13T00:51:07Z |
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spelling | doaj.art-65f493262d5547038186a18b458130932022-12-22T03:09:53ZengMDPI AGMarine Drugs1660-33972019-07-0117844410.3390/md17080444md17080444Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling PathwayAo Xuan Zhen0Yu Jae Hyun1Mei Jing Piao2Pincha Devage Sameera Madushan Fernando3Kyoung Ah Kang4Mee Jung Ahn5Joo Mi Yi6Hee Kyoung Kang7Young Sang Koh8Nam Ho Lee9Jin Won Hyun10School of Medicine, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaLaboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 63243, KoreaDepartment of Microbiology and Immunology, College of Medicine, Inje University, Busan 47392, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaDepartment of Chemistry and Cosmetics, College of Natural Sciences, Jeju National University, Jeju 63243, KoreaSchool of Medicine, Jeju National University, Jeju 63243, KoreaToxicity of particulate matter (PM) towards the epidermis has been well established in many epidemiological studies. It is manifested in cancer, aging, and skin damage. In this study, we aimed to show the mechanism underlying the protective effects of eckol, a phlorotannin isolated from brown seaweed, on human HaCaT keratinocytes against PM<sub>2.5</sub>-induced cell damage. First, to elucidate the underlying mechanism of toxicity of PM<sub>2.5</sub>, we checked the reactive oxygen species (ROS) level, which contributed significantly to cell damage. Experimental data indicate that excessive ROS caused damage to lipids, proteins, and DNA and induced mitochondrial dysfunction. Furthermore, eckol (30 μM) decreased ROS generation, ensuring the stability of molecules, and maintaining a steady mitochondrial state. The western blot analysis showed that PM<sub>2.5</sub> promoted apoptosis-related protein levels and activated MAPK signaling pathway, whereas eckol protected cells from apoptosis by inhibiting MAPK signaling pathway. This was further reinforced by detailed investigations using MAPK inhibitors. Thus, our results demonstrated that inhibition of PM<sub>2.5</sub>-induced cell apoptosis by eckol was through MAPK signaling pathway. In conclusion, eckol could protect skin HaCaT cells from PM<sub>2.5</sub>-induced apoptosis via inhibiting ROS generation.https://www.mdpi.com/1660-3397/17/8/444phlorotanninparticulate matterreactive oxygen specieskeratinocytes |
spellingShingle | Ao Xuan Zhen Yu Jae Hyun Mei Jing Piao Pincha Devage Sameera Madushan Fernando Kyoung Ah Kang Mee Jung Ahn Joo Mi Yi Hee Kyoung Kang Young Sang Koh Nam Ho Lee Jin Won Hyun Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway Marine Drugs phlorotannin particulate matter reactive oxygen species keratinocytes |
title | Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway |
title_full | Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway |
title_fullStr | Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway |
title_full_unstemmed | Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway |
title_short | Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway |
title_sort | eckol inhibits particulate matter 2 5 induced skin keratinocyte damage via mapk signaling pathway |
topic | phlorotannin particulate matter reactive oxygen species keratinocytes |
url | https://www.mdpi.com/1660-3397/17/8/444 |
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