Astragaloside IV controls collagen reduction in photoaging skin by improving transforming growth factor-β/Smad signaling suppression and inhibiting matrix metalloproteinase-1

Exposure to ultraviolet (UV) light reduces levels of type I collagen in the dermis and results in human skin damage and premature skin aging (photoaging). This leads to a wrinkled appearance through the inhibition of transforming growth factor-beta (TGF-beta)/Smad signaling. UV irradiation increases type I collagen degradation through upregulating matrix metalloproteinase (MMP) expression. Astragaloside IV (AST) is one of the major active components extracted from Astragalus membranaceus. However, its multiple anti-photoaging effects remain to be elucidated. In the present study, the effects of AST against collagen reduction in UV-induced skin aging in human skin fibroblasts were investigated. The expression of type I procollagen (COL1), MMP-1, TGF-beta RII and Smad7 were determined using reverse transcription-polymerase chain reaction, western blotting and ELISA, respectively. UV irradiation inhibits type I collagen production by suppressing the TGF-beta/Smad signaling pathway and increasing COL1 degradation by inducing MMP-1 expression. Transforming growth factor-beta type II protein and COL1 mRNA decreased but MMP-1 and Smad7 levels increased in the photoaging model group, which was reversed by topical application of AST. AST prevents collagen reduction from UV irradiation in photoaging skin by improving TGF-beta/Smad signaling suppression and inhibiting MMP-1, thus AST may be a potential agent against skin photoaging.