Abstract

In this study, we aim to investigate the protective effects of astragaloside on ultraviolet A (UVA)-induced photoaging in human fibroblasts and its possible mechanisms. Subconfluent fibroblasts were cultured and divided into normal control group, astragaloside group, UVA irradiation group and UVA plus astragaloside group. The cells were shammed or irradiated with 10 J/cm(2) of UVA irradiation and treated with 20 μg/mL astragaloside. The aging condition was determined by histochemical staining of senescence-associated β-galactosidase (SA-β-gal). Concentration of transforming growth factor-β1 (TGF-β1) in the supernatant was determined by enzyme-linked immunosorbent assay, and mRNA levels of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were measured by real-time polymerase chain reaction. UVA irradiation raised the proportion of SA-β-gal-positive cells in comparison with the normal control group (P<0.05). Astragaloside treatment was shown to decrease the level of SA-β-gal compared with the UVA group. With UVA irradiation, the concentration of TGF-β1 in the supernatant decreased, and astragaloside treatment recovered the content of TGF-β1 compared with the UVA irradiation alone (P<0.05). UVA irradiation also up-regulated the mRNA levels of MMP-1 and TIMP-1 (P<0.05). Astragaloside decreased the mRNA level of MMP-1 compared with the UVA irradiation alone, while the TIMP-1 expression increased (P<0.05). Astragaloside can protect the skin from UVA irradiation. The mechanism involved may be related with TGF secretion and decrease of collagen degradation.

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