Protective and Reparative Effects of Tremella aurantialba Extract against Skin Photoaging and Its Underlying Mechanisms

TL;DR

This study explores how Tremella aurantialba extract protects skin from UV-induced aging and identifies the mechanisms behind its effects.

Contribution

The study reveals the multi-targeted protective effects of T. aurantialba extract against skin photoaging through metabolomics and microbiome analysis.

Findings

TAE reduces UVB-induced cell damage and ROS levels in HaCaT cells.

TAE restores collagen fibers and balances skin microbiota in UVA/UVB-exposed mice.

TAE modulates lipid metabolism and circadian rhythm genes to mitigate photoaging.

Abstract

While Tremella aurantialba (T. aurantialba) is known for its significant antioxidant and anti-inflammatory activities, its role in skin photoaging remains unclear. In this study, we elucidated the protective mechanisms of T. aurantialba extract (TAE) against ultraviolet A and ultraviolet B (UVA/UVB)-induced skin photoaging. Using UHPLC-Q-Orbitrap-MS analysis, a total of 24 compounds were identified from TAE, including trigonelline (22.83%), isonicotinic acid (18.16%), acetylcholine (16.66%), choline (15.02%), and 2-hydroxyphenylalanine (6.85%). In vitro investigations revealed that TAE significantly enhanced the survival rate of UVB-induced HaCaT cells, promoted cell migration, and increased the migration rates to above 50%, while concurrently reducing reactive oxygen species (ROS) levels. In vivo, TAE suppressed abnormal epidermal thickening and mast cell infiltration induced by UVA/UVB in the dorsal skin of mice, and facilitated the restoration of collagen fibers. Metabolomics analysis indicated that TAE mitigated photoaging mainly by modulating the sphingolipid and glycerophospholipid metabolic pathways. Skin microbiome analysis showed that TAE boosts Bacillota and Bacteroidota while suppressing Exiguobacterium and Lachnospiraceae, consequently restoring skin microbiota balance and facilitating skin repair. Transcriptome analysis demonstrated that genes modulated by TAE were primarily concentrated in lipid metabolism, circadian rhythm, and response to oxygen-containing compounds. This suggests TAE facilitated skin barrier repair and mitigated UVA/UVB-induced photoaging by modulating cellular physiological rhythms and lipid metabolism, while controlling oxidative stress. In conclusion, TAE mitigates UVA/UVB-induced damage via multi-targeted antioxidant, anti-inflammatory, and skin barrier repair-promoting effects, thereby establishing a scientific basis for its application in developing functional foods and cosmetics to target photoaging.

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