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

Kyoung Ah Kang, Kyoung Hwa Lee, Sungwook Chae, Rui Zhang, Myung Sun Jung, Youngki Lee, So Young Kim, Hee Sun Kim, Hong Gu Joo, Jae Woo Park, Young Min Ham, Nam Ho Lee, Jin Won Hyun

Research output: Contribution to journalArticlepeer-review

139 Scopus citations


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 (H2O 2), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, eckol reduced H 2O2 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 κ 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.

Original languageEnglish
Pages (from-to)6295-6304
Number of pages10
JournalFEBS Letters
Issue number28
StatePublished - 21 Nov 2005

Bibliographical note

Funding Information:
This study was supported by a grant from Korea Science and Engineering Foundation (KOSEF), and Ministry of Science and Technology (MOST), Korean government, and in part by a grant from the Cheju National University Development Foundation.


  • Apoptosis
  • Catalase
  • Eckol
  • Oxidative stress
  • Signal pathway


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