Effect and Mechanism of Tricholoma matsutake Extract on UVA and UVB Radiation-Induced Skin Aging
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Ultraviolet (UV) radiation often causes skin aging, inflammation, cancer and other related skin diseases. In this study, the main components of Tricholoma matsutake extract (TME) were identified using UPLC-Q-TOF-MS, and their anti-photoaging effects were assessed through UV-induced cell and animal models. The key components identified were D-mannitol (27.41%), DL-malic acid (14%), alginate (12.5%), isoleucine (4.82%), and phenylalanine (4.31%), all of which played roles in antiaging and UV protection. TME (50-100 mg/ml) significantly alleviated UVA/UVB-induced erythema and wrinkles in mice. Pathological staining showed that TME suppressed UV-induced epidermal hyperplasia (p < 0.05), reduced collagen damage (p < 0.01), and decreased mast cell infiltration (p < 0.01), while down-regulating inflammatory markers such as IL-6, IL-1β, and TNF-α. TME also upregulated type I collagen (COL-1). Flow cytometry results demonstrated that high-dose TME inhibited UV-induced apoptosis and reduced reactive oxygen species (ROS) in HaCaT cells (p < 0.05). Immunofluorescence and scratch migration assays showed that TME promoted PPAR-α expression, reduced inflammation, and supported skin repair (p < 0.01). Transcriptomic and metabolomic analyses indicated that TME regulated inflammation-related signaling pathways, helping to prevent skin aging. TME is a promising natural product for skin care and treatment of oxidative stress and inflammation-related diseases.
Abstract
Ultraviolet (UV) radiation often causes skin aging, inflammation, cancer and other related skin diseases. In this study, the main components of Tricholoma matsutake extract (TME) were identified using UPLC-Q-TOF-MS, and their anti-photoaging effects were assessed through UV-induced cell and animal models. The key components identified were D-mannitol (27.41%), DL-malic acid (14%), alginate (12.5%), isoleucine (4.82%), and phenylalanine (4.31%), all of which played roles in antiaging and UV protection. TME (50-100 mg/ml) significantly alleviated UVA/UVB-induced erythema and wrinkles in mice. Pathological staining showed that TME suppressed UV-induced epidermal hyperplasia (p < 0.05), reduced collagen damage (p < 0.01), and decreased mast cell infiltration (p < 0.01), while down-regulating inflammatory markers such as IL-6, IL-1β, and TNF-α. TME also upregulated type I collagen (COL-1). Flow cytometry results demonstrated that high-dose TME inhibited UV-induced apoptosis and reduced reactive oxygen species (ROS) in HaCaT cells (p < 0.05). Immunofluorescence and scratch migration assays showed that TME promoted PPAR-α expression, reduced inflammation, and supported skin repair (p < 0.01). Transcriptomic and metabolomic analyses indicated that TME regulated inflammation-related signaling pathways, helping to prevent skin aging. TME is a promising natural product for skin care and treatment of oxidative stress and inflammation-related diseases.