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

Abstract

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 findings strongly suggest that PM is a promising inhibitor of skin photoaging.

A Peptide YGDEY from Tilapia Gelatin Hydrolysates Inhibits UVB‐mediated Skin Photoaging by Regulating MMP‐1 and MMP‐9 Expression in HaCaT Cells

“…The MAPK signaling pathway is involved in cellular changes such as cell growth, apoptosis and regulation of inflammatory response . To determine the effect of YGDEY on MAPK and NF‐ κ B signal pathway in UVB‐induced cells, the Western blotting analysis and p65 translocation were conducted.…”

“…NF‐ κ B is a transcription factor of human skin and composed of p50/p65 subunits to form heterodimer and it can be activated via MAPK. Moreover, the promoter of MMP‐1, MMP‐3 and MMP‐9 gene contain active site that binds to NF‐ κ B . Therefore, NF‐ κ B and MAPK signaling pathways play an important role in the process of collagen degradation.…”

Potential Molecular Mechanisms of Plantain in the Treatment of Gout and Hyperuricemia Based on Network Pharmacology

“…Therefore, RAGE is critical in the development of hyperuricemia and gout diseases. Experiments showed that, in the human keratinocyte cell line (HaCaT) and primary human dermal fibroblasts (HDF) cell experiments, plantain could reduce the expression of MMP-1 and proinflammatory cytokines induced by ultraviolet radiation B (UVB) and AGEs by inhibiting the phosphorylation of MAPKs, reduce the NF- κ B nuclear translocation by inhibiting the I κ B α phosphorylation, and reduce upregulation of RAGE [ 80 ]. In summary, the AGE-RAGE signaling pathway in diabetic complications may be an effective way for plantain to treat gouty arthritis.…”

Plantamajoside from Plantago asiatica modulates human umbilical vein endothelial cell dysfunction by glyceraldehyde-induced AGEs via MAPK/NF-κB

“…Our groups have reported that glycolaldehyde-derived AGEs stimulated intracellular ROS production and pro-inflammatory mediators including TNF-α and IL-1β via the AGE-RAGE axis [39]. One recent study showed that co-treatment with PM and glycer-AGEs in keratinocytes and fibroblasts inhibits UVB-irradiation- and AGE-induced RAGE overexpression and proinflammatory cytokine expression via attenuating MAPK activation by ROS [40]. Given that PM is absorbed very rapidly into the blood in rats after oral administration of P. asiatica extract [41], in the present study, we co-treated PM with glycer-AGEs in HUVECs to inhibit intracellular ROS production via AGE-RAGE interaction.…”