Biomol Ther.  2024 Jul;32(4):499-507. 10.4062/biomolther.2024.054.

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

• Lim C
• Piao MJ
• Kang KA
• Fernando PDSM
• Herath HMUL
• Kim DW
• Yi JM
• Choi YH
• Hyun JW

• KMID: 2557199
• DOI: http://doi.org/10.4062/biomolther.2024.054

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.

Keyword

1,3,5-Trihydroxybenzene; Ultraviolet B; NADPH oxidase; AMP-activated protein kinase; c-Jun N-terminal kinase