Resumen
Ultraviolet A (UVA)-induced detrimental effects in the skin, also known as photoaging, are mediated with several pathways including oxidative stress generation and extracellular matrix (ECM) degradation. UVA irradiation results in excessive production of matrix metalloproteinases (MMPs), enzymes responsible for the degradation of ECM components such as collagen. In this study, the protective effects of (2'S)-columbianetin against UVA-induced changes in matrix metalloproteinase-1 (MMP-1) and collagen production were investigated in human dermal fibroblasts (HDFs). The (2'S)-columbianetin was isolated from Corydalis heterocarpa. UVA exposure increased MMP-1 release from HDFs and diminished the release of type I pro-collagen. Treatment with (2'S)-columbianetin reversed these effects of UVA exposure. The (2'S)-columbianetin treatment also suppressed the intracellular expression of MMP-1 and increased type I pro-collagen expression. UVA exposure elevated the activation of p38, c-Jun-amino-terminal kinase (JNK) and extracellular signal-related kinase (ERK) as the mechanism to stimulate MMP-1 production. The (2'S)-columbianetin suppressed the phosphorylation of JNK and ERK. The (2'S)-columbianetin was also stimulated collagen production via TGFß signaling cascade, relieving UVA-induced suppression of Smad2/3 phosphorylation and translocation. In conclusion, (2'S)-columbianetin was suggested to be a potential cosmeceutical lead compound with antiphotoaging properties against UVA-induced collagen degradation.