Biomolecules & Therapeutics  
Purpurogallin Protects Keratinocytes from Damage and Apoptosis Induced by Ultraviolet B Radiation and Particulate Matter 2.5
Ao Xuan Zhen1, Mei Jing Piao1, Yu Jae Hyun1, Kyoung Ah Kang1, Yea Seong Ryu1, Suk Ju Cho1,Hee Kyoung Kang1, Young Sang Koh1, Mee Jung Ahn2, Tae Hoon Kim3 and Jin Won Hyun1,*
1Jeju National University School of Medicine and Jeju Research Center for Natural Medicine, Jeju 63243,
2Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 63243,
3Department of Food Science and Biotechnology, Daegu University, Gyeongsan 38453, Republic of Korea
E-mail: jinwonh@jejunu.ac.kr
Tel: +82-64-754-3838, Fax: +82-64-702-2687
Received: August 7, 2018; Revised: September 13, 2018; Accepted: October 6, 2018; Published online: November 12, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Purpurogallin, a natural phenol obtained from oak nutgalls, has been shown to possess antioxidant, anticancer, and anti-inflammatory effects. Recently, in addition to ultraviolet B (UVB) radiation that induces cell apoptosis via oxidative stress, particulate matter 2.5 (PM2.5) was shown to trigger excessive production of reactive oxygen species. In this study, we observed that UVB radiation and PM2.5 severely damaged human HaCaT keratinocytes, disrupting cellular DNA, lipids, and proteins and causing mitochondrial depolarization. Purpurogallin protected HaCaT cells from apoptosis induced by UVB radiation and/or PM2.5. Furthermore, purpurogallin effectively modulates the pro-apoptotic and anti-apoptotic proteins under UVB irradiation via caspase signaling pathways. Additionally, purpurogallin reduced apoptosis via MAPK signaling pathways, as demonstrated using MAPK-p38, ERK, and JNK inhibitors. These results indicate that purpurogallin possesses antioxidant effects and protects cells from damage and apoptosis induced by UVB radiation and PM2.5.
Keywords: Purpurogallin, Ultraviolet B radiation, Particulate matter 2.5, Oxidative stress, Human HaCaT keratinocytes


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