Plantamajoside Inhibits UVB and Advanced Glycation End Products‐Induced MMP ‐1 Expression by Suppressing the MAPK and NF‐ κ B Pathways in HaCaT Cells

Photoaging and glycation stress are major causes of skin deterioration. Oxidative stress caused by ultraviolet B ( UVB ) irradiation can upregulate matrix metalloprotease 1 ( MMP ‐1), a major enzyme responsible for collagen damage in the skin. Advanced glycation end products ( AGE s) accumulate via gradual formation from skin proteins, especially from long‐lived proteins such as dermal elastin and collagen. Plantamajoside ( PM ), isolated from Plantago asiatica , has various biological effects including anti‐inflammatory and antioxidant effects. In this study, we assessed the protective effects of PM on a human keratinocyte cell line (HaCaT) and primary human dermal fibroblasts ( HDF ) against stress caused by glyceraldehyde‐induced AGE s (glycer‐ AGE s) with UVB irradiation. We found that PM attenuated UVB ‐ and‐glycer‐ AGE s‐induced MMP ‐1 expression in HaCaT and HDF cells and proinflammatory cytokines expression by inhibiting the phosphorylation of mitogen‐activated protein kinases ( MAPK s) activated by reactive oxygen species. Specific inhibitors of NF ‐ κ B and MAPK s attenuated the induced expression of MMP ‐1. PM also inhibited the phosphorylation of I κ B α , and reduced nuclear translocation of NF ‐ κ B in these cells. Furthermore, PM attenuated the upregulation of receptor for AGE s ( RAGE ) by glycer‐ AGE s with UVB irradiation. Therefore, our findings strongly suggest that PM is a promising inhibitor of skin photoaging.