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Niacinamide Protects Skin Cells from Oxidative Stress Induced by Particulate Matter

  • Zhen, Ao Xuan (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Piao, Mei Jing (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Kang, Kyoung Ah (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Fernando, Pincha Devage Sameera Madushan (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Kang, Hee Kyoung (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Koh, Young Sang (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Yi, Joo Mi (Department of Microbiology and Immunology, Inje University College of Medicine) ;
  • Hyun, Jin Won (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine)
  • Received : 2019.04.15
  • Accepted : 2019.06.07
  • Published : 2019.11.01

Abstract

Niacinamide (NIA) is a water-soluble vitamin that is widely used in the treatment of skin diseases. Moreover, NIA displays antioxidant effects and helps repair damaged DNA. Recent studies showed that particulate matter 2.5 ($PM_{2.5}$) induced reactive oxygen species (ROS), causing disruption of DNA, lipids, and protein, mitochondrial depolarization, and apoptosis of skin keratinocytes. Here, we investigated the protective effects of NIA on $PM_{2.5}$-induced oxidative stress in human HaCaT keratinocytes. We found that NIA could inhibit the ROS generation induced by $PM_{2.5}$, as well block the $PM_{2.5}$-induced oxidation of molecules, such as lipids, proteins, and DNA. Furthermore, NIA alleviated $PM_{2.5}$-induced accumulation of cellular $Ca^{2+}$, which caused cell membrane depolarization and apoptosis, and reduced the number of apoptotic cells. Collectively, the findings show that NIA can protect keratinocytes from $PM_{2.5}$-induced oxidative stress and cell damage.

Keywords

References

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