Cedrol prevents UVB-induced photoaging by restoring mitochondrial function, metabolic homeostasis, and skin barrier integrity in HaCaT cells.

Abstract

Context: Ultraviolet B (UVB) radiation is a key environmental contributor to skin photoaging, primarily by inducing oxidative stress, mitochondrial dysfunction, metabolic imbalance, and downregulation of tight junction (TJ) proteins. Cedrol, the major component of the essential oil from Cunninghamia lanceolata var. konishii, a tree species endemic to Taiwan, exhibits antioxidant properties. However, its restorative effects against UVB-induced skin damage have not been fully elucidated.

Objective: In this study, HaCaT keratinocytes were used to evaluate the post-treatment effects of cedrol on UVB-induced damage to skin cells.

Materials and methods: HaCaT cells were exposed to UVB irradiation followed by cedrol treatment. Cell viability, intracellular reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, mitochondrial biogenesis-related proteins (SIRT1, PGC-1α, Nrf2, TFAM), and TJ proteins (ZO-1, occludin, claudin-3) were assessed. Additionally, ¹H-NMR-based metabolomics was conducted to evaluate UVB-induced metabolic changes.

Results: Cedrol significantly improved cell viability post-UVB exposure, decreased intracellular reactive oxygen species (ROS), and restored mitochondrial membrane potential and ATP levels. It also upregulated mitochondrial biogenesis-related proteins (SIRT1, PGC-1α, Nrf2, and TFAM) and maintained TJ protein expression (ZO-1, occludin, and claudin-3), thereby preserving epithelial barrier integrity. Furthermore, ¹H-NMR-based metabolomics revealed that cedrol mitigated UVB-induced metabolic disturbances, particularly in amino acid and energy pathways.

Discussion and conclusion: Cedrol alleviates UVB-induced cellular damage by modulating mitochondrial function and metabolic homeostasis, indicating its potential as a natural agent for promoting skin recovery after UV exposure.