4.5 Article

Photoprotective Potential of Penta-O-Galloyl-β-D-Glucose by Targeting NF-κB and MAPK Signaling in UVB Radiation-Induced Human Dermal Fibroblasts and Mouse Skin

Journal

MOLECULES AND CELLS
Volume 38, Issue 11, Pages 982-990

Publisher

KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.14348/molcells.2015.0169

Keywords

1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG); inflammation; mitogen-activated protein kinase (MAPK); nuclear factor-kappaB (NF-kappa B); reactive oxygen species (ROS); ultraviolet B (UVB)

Funding

  1. National Research Foundation of Korea (NRF) - Korea government (MSIP) [2012R1A5A2A44671346]
  2. National Research Foundation of Korea (NRF) - Korea government (MESF) [2014R 1A2A1A11053203]
  3. National R&D program for Cancer Control, Ministry of Health & Welfare, Republic of Korea [0720540]
  4. Seoul National University Hospital (SNUH) Research Fund [3420130270, 0320140100]

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Exposure of the skin to ultraviolet radiation can cause skin damage with various pathological changes including inflammation. In the present study, we identified the skinprotective activity of 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (pentagalloyl glucose, PGG) in ultraviolet B (UVB) radiation-induced human dermal fibroblasts and mouse skin. PGG exhibited antioxidant activity with regard to intracellular reactive oxygen species (ROS) generation as well as ROS and reactive nitrogen species (RNS) scavenging. Furthermore, PGG exhibited anti-inflammatory activity, inhibiting the activation of nuclear factor-kappaB (NF-kappa B) and mitogen-activated protein kinase (MAPK) signaling, resulting in inhibition of the expression of pro-inflammatory mediators. Topical application of PGG followed by chronic exposure to UVB radiation in the dorsal skin of hairless mice resulted in a significant decrease in the progression of inflammatory skin damages, leading to inhibited activation of NF-kappa B signaling and expression of pro-inflammatory mediators. The present study demonstrated that PGG protected from skin damage induced by UVB radiation, and thus, may be a potential candidate 1 for the prevention of environmental stimuli-induced inflammatory skin damage.

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