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

doi:10.1016/j.febslet.2005.10.008

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

Department of Molecular Medicine

Research output: Contribution to journal › Article › peer-review

143 Scopus citations

Abstract

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 language	English
Pages (from-to)	6295-6304
Number of pages	10
Journal	FEBS Letters
Volume	579
Issue number	28
DOIs	https://doi.org/10.1016/j.febslet.2005.10.008
State	Published - 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.

Keywords

Apoptosis
Catalase
Eckol
Oxidative stress
Signal pathway

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10.1016/j.febslet.2005.10.008

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title = "Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in lung fibroblast cells",

abstract = "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.",

keywords = "Apoptosis, Catalase, Eckol, Oxidative stress, Signal pathway",

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

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.",

year = "2005",

month = nov,

day = "21",

doi = "10.1016/j.febslet.2005.10.008",

language = "English",

volume = "579",

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journal = "FEBS Letters",

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TY - JOUR

T1 - Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in lung fibroblast cells

AU - Kang, Kyoung Ah

AU - Lee, Kyoung Hwa

AU - Chae, Sungwook

AU - Zhang, Rui

AU - Jung, Myung Sun

AU - Lee, Youngki

AU - Kim, So Young

AU - Kim, Hee Sun

AU - Joo, Hong Gu

AU - Park, Jae Woo

AU - Ham, Young Min

AU - Lee, Nam Ho

AU - Hyun, Jin Won

N1 - 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.

PY - 2005/11/21

Y1 - 2005/11/21

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Catalase

KW - Eckol

KW - Oxidative stress

KW - Signal pathway

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

Abstract

Bibliographical note

Keywords

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