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Inhibitory Action of 1,3,5-Trihydroxybenzene on UVB-Induced NADPH Oxidase 4 through AMPK and JNK Signaling Pathways

  • Chaemoon Lim (Department of Orthopedic Surgery, Jeju National University Hospital, College of Medicine, Jeju National University) ;
  • Mei Jing Piao (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Kyoung Ah Kang (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Pincha Devage Sameera Madushan Fernando (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Herath Mudiyanselage Udari Lakmini Herath (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Dae Whan Kim (Department of Orthopedic Surgery, Jeju National University Hospital, College of Medicine, Jeju National University) ;
  • Joo Mi Yi (Department of Microbiology and Immunology, Inje University College of Medicine) ;
  • Yung Hyun Choi (Department of Biochemistry, College of Oriental Medicine, Dongeui University) ;
  • Jin Won Hyun (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University)
  • Received : 2024.04.03
  • Accepted : 2024.05.24
  • Published : 2024.07.01

Abstract

Specific sensitivity of the skin to ultraviolet B (UVB) rays is one of the mechanisms responsible for widespread skin damage. This study tested whether 1,3,5-trihydroxybenzene (THB), a compound abundant in marine products, might inhibit UVB radiationinduced NADPH oxidase 4 (NOX4) in both human HaCaT keratinocytes and mouse dorsal skin and explore its cytoprotective mechanism. The mechanism of action was determined using western blotting, immunocytochemistry, NADP+/NADPH assay, reactive oxygen species (ROS) detection, and cell viability assay. THB attenuated UVB-induced NOX4 expression both in vitro and in vivo, and suppressed UVB-induced ROS generation via NADP+ production, resulting in increased cell viability with decreased apoptosis. THB also reduced the expression of UVB-induced phosphorylated AMP-activated protein kinase (AMPK) and phosphorylated c-Jun N-terminal kinase (JNK). THB suppressed UVB-induced NOX4 expression and ROS generation by inhibiting AMPK and JNK signaling pathways, thereby inhibiting cellular damage. These results showed that THB could be developed as a UV protectant.

Keywords

Acknowledgement

This work was supported by a research grant from Jeju National University Hospital in 2022.

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