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Open AccessArticle

Particulate Matter 2.5 Mediates Cutaneous Cellular Injury by Inducing Mitochondria-Associated Endoplasmic Reticulum Stress: Protective Effects of Ginsenoside Rb1

1
Jeju Research Center for Natural Medicine, Jeju National University School of Medicine, Jeju 63243, Korea
2
Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 63243, Korea
3
Department of Microbiology and Immunology, Inje University College of Medicine, Busan 47392, Korea
4
Department of Biochemistry, College of Oriental Medicine, Dongeui University, Busan 47340, Korea
*
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(9), 383; https://doi.org/10.3390/antiox8090383
Received: 26 July 2019 / Revised: 25 August 2019 / Accepted: 8 September 2019 / Published: 9 September 2019
The prevalence of fine particulate matter-induced harm to the human body is increasing daily. The aim of this study was to elucidate the mechanism by which particulate matter 2.5 (PM2.5) induces damage in human HaCaT keratinocytes and normal human dermal fibroblasts, and to evaluate the preventive capacity of the ginsenoside Rb1. PM2.5 induced oxidative stress by increasing the production of reactive oxygen species, leading to DNA damage, lipid peroxidation, and protein carbonylation; this effect was inhibited by ginsenoside Rb1. Through gene silencing of endoplasmic reticulum (ER) stress-related genes such as PERK, IRE1, ATF, and CHOP, and through the use of the ER stress inhibitor tauroursodeoxycholic acid (TUDCA), it was demonstrated that PM2.5-induced ER stress also causes apoptosis and ultimately leads to cell death; however, this phenomenon was reversed by ginsenoside Rb1. We also found that TUDCA partially restored the production of ATP that was inhibited by PM2.5, and its recovery ability was significantly higher than that of ginsenoside Rb1, indicating that the process of ER stress leading to cell damage may also occur via the mitochondrial pathway. We concluded that ER stress acts alone or via the mitochondrial pathway in the induction of cell damage by PM2.5, and that ginsenoside Rb1 blocks this process. Ginsenoside Rb1 shows potential for use in skin care products to protect the skin against damage by fine particles. View Full-Text
Keywords: particulate matter 2.5; ginsenoside Rb1; endoplasmic reticulum stress; oxidative stress; apoptosis particulate matter 2.5; ginsenoside Rb1; endoplasmic reticulum stress; oxidative stress; apoptosis
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Piao, M.J.; Kang, K.A.; Zhen, A.X.; Fernando, P.D.S.M.; Ahn, M.J.; Koh, Y.S.; Kang, H.K.; Yi, J.M.; Choi, Y.H.; Hyun, J.W. Particulate Matter 2.5 Mediates Cutaneous Cellular Injury by Inducing Mitochondria-Associated Endoplasmic Reticulum Stress: Protective Effects of Ginsenoside Rb1. Antioxidants 2019, 8, 383.

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