Abstract

Ultraviolet B (UVB)-induced photoaging is characterized by oxidative stress, mitochondrial dysfunction, and epidermal barrier impairment. Although extracellular vesicles (EVs) have emerged as bioactive mediators of intercellular signaling, the dermatological relevance of fungal-derived EVs remains poorly understood. In this study, we investigated whether EVs isolated from liquid-cultured Taiwanofungus camphoratus mycelia (TCEVs) protect keratinocytes against UVB-induced damage. TCEVs displayed nanosized vesicular features with a mean particle size of 134.6 ± 4.6 nm and a stable negative surface charge. In HaCaT cells, TCEVs showed no obvious cytotoxicity and increased wound closure. In UVB-exposed keratinocytes, TCEV pretreatment improved cell viability, increased ATP production, reduced intracellular reactive oxygen species accumulation, and improved mitochondrial membrane potential. At the highest tested concentration (10 × 1010 particles/mL), TCEVs reduced UVB-induced relative ROS levels from 118.65% to 98.2% and increased relative ATP levels from 70.47% to 86.0%. TCEVs also increased the expression of ZO-1, occludin, and Claudin-3 and were associated with increased SIRT1 and p-AMPK expression and partial improvement of PGC-1α. In contrast, Nrf2 and TFAM did not differ significantly from the UVB-irradiated group. These findings support the potential of TCEVs to prevent UVB-induced keratinocyte damage under the present in vitro conditions.

IPC Classification

Keywords