Plantamajoside inhibits UVB and advanced glycation end products-induced MMP-1 expression. - GreenMedInfo Summary
Plantamajoside Inhibits UVB and Advanced Glycation End Products-Induced MMP-1 Expression by Suppressing the MAPK and NF-κB Pathways in HaCaT Cells.
Photochem Photobiol. 2016 09 ;92(5):708-19. Epub 2016 Aug 9. PMID: 27346084
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 (AGEs) 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 AGEs (glycer-AGEs) with UVB irradiation. We found that PM attenuated UVB- and-glycer-AGEs-induced MMP-1 expression in HaCaT and HDF cells and proinflammatory cytokines expression by inhibiting the phosphorylation of mitogen-activated protein kinases (MAPKs) activated by reactive oxygen species. Specific inhibitors of NF-κB and MAPKs attenuated the induced expression of MMP-1. PM also inhibited the phosphorylation of IκBα, and reduced nuclear translocation of NF-κB in these cells. Furthermore, PM attenuated the upregulation of receptor for AGEs (RAGE) by glycer-AGEs with UVB irradiation. Therefore, our findingsstrongly suggest that PM is a promising inhibitor of skin photoaging.