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Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in lung fibroblast cells
Author(s) -
Kang Kyoung Ah,
Lee Kyoung Hwa,
Chae Sungwook,
Zhang Rui,
Jung Myung Sun,
Lee Youngki,
Kim So Young,
Kim Hee Sun,
Joo Hong Gu,
Park Jae Woo,
Ham Young Min,
Lee Nam Ho,
Hyun Jin Won
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.10.008
Subject(s) - oxidative stress , catalase , reactive oxygen species , lipid peroxidation , extracellular , chemistry , fibroblast , intracellular , cell damage , oxidative phosphorylation , antioxidant , biochemistry , microbiology and biotechnology , cell culture , biology , in vitro , genetics
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 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.