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Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage
Published on: February 15, 2020
Protective effects of astragaloside against ultraviolet A-induced photoaging in human fibroblasts
1Department of Dermatology, Jiangsu Province Official Hospital, Nanjing 210024, Jiangsu Province, China;
Objective:
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.
Methods:
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.
Results:
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).
Conclusion:
Astragaloside can protect the skin from UVA irradiation. The mechanism involved may be related with TGF secretion and decrease of collagen degradation.