Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in lung fibroblast cells

FEBS Lett. 2005 Nov 21;579(28):6295-304. doi: 10.1016/j.febslet.2005.10.008. Epub 2005 Oct 19.


We have investigated the cytoprotective effect of eckol, which was isolated from Ecklonia cava, against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Eckol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl radical, hydrogen peroxide (H(2)O(2)), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, eckol reduced H(2)O(2) induced cell death in V79-4 cells. In addition, eckol inhibited cell damage induced by serum starvation and radiation by scavenging ROS. Eckol was found to increase the activity of catalase and its protein expression. Further, molecular mechanistic study revealed that eckol increased phosphorylation of extracellular signal-regulated kinase and activity of nuclear factor kappa B. Taken together, the results suggest that eckol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Catalase / drug effects
  • Cell Line
  • Cricetinae
  • Dioxins / isolation & purification
  • Dioxins / pharmacology*
  • Extracellular Signal-Regulated MAP Kinases / drug effects
  • Fibroblasts / drug effects*
  • Fibroblasts / enzymology
  • Free Radical Scavengers / isolation & purification
  • Free Radical Scavengers / pharmacology*
  • Lipid Peroxidation / drug effects
  • Lung / cytology
  • Oxidative Stress / drug effects*
  • Phaeophyceae / chemistry*
  • Phosphorylation / drug effects
  • Reactive Oxygen Species / metabolism
  • Transcription Factor RelA / metabolism


  • Dioxins
  • Free Radical Scavengers
  • Reactive Oxygen Species
  • Transcription Factor RelA
  • eckol
  • Catalase
  • Extracellular Signal-Regulated MAP Kinases