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