Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

Kyoung Ah Kang; Rui Zhang; Mei Jing Piao; Kyoung Hwa Lee; Bum Joon Kim; So Young Kim; Hee Sun Kim; Dong Hyun Kim; Ho Jin You; Jin Won Hyun

doi:10.1080/10715760701241618

Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

Kyoung Ah Kang
, Rui Zhang
, Mei Jing Piao
, Kyoung Hwa Lee
, Bum Joon Kim
, So Young Kim
, Hee Sun Kim
, Dong Hyun Kim
, Ho Jin You
, Jin Won Hyun

Department of Molecular Medicine

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

34 Scopus citations

Abstract

The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H₂O₂) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H₂O₂ treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H₂O₂ induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.

Original language	English
Pages (from-to)	720-729
Number of pages	10
Journal	Free Radical Research
Volume	41
Issue number	6
DOIs	https://doi.org/10.1080/10715760701241618
State	Published - 2007

Bibliographical note

Funding Information:
This research was supported by the study of the DNA repair regulation with disease program and by the program of Basic Atomic Energy Research Institute (BAERI) which is a part of the Nuclear R&D programs grant from the Ministry of Science and Technology of Korea.

Keywords

Cytoprotective properties
Glycitein
Oxidative stress
Reactive oxygen species

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10.1080/10715760701241618

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title = "Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase",

abstract = "The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H2O2 treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H2O2 induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.",

keywords = "Cytoprotective properties, Glycitein, Oxidative stress, Reactive oxygen species",

author = "Kang, \{Kyoung Ah\} and Rui Zhang and Piao, \{Mei Jing\} and Lee, \{Kyoung Hwa\} and Kim, \{Bum Joon\} and Kim, \{So Young\} and Kim, \{Hee Sun\} and Kim, \{Dong Hyun\} and You, \{Ho Jin\} and Hyun, \{Jin Won\}",

note = "Funding Information: This research was supported by the study of the DNA repair regulation with disease program and by the program of Basic Atomic Energy Research Institute (BAERI) which is a part of the Nuclear R\&D programs grant from the Ministry of Science and Technology of Korea.",

year = "2007",

doi = "10.1080/10715760701241618",

language = "English",

volume = "41",

pages = "720--729",

journal = "Free Radical Research",

issn = "1071-5762",

publisher = "Taylor and Francis Ltd.",

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TY - JOUR

T1 - Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

AU - Kang, Kyoung Ah

AU - Zhang, Rui

AU - Piao, Mei Jing

AU - Lee, Kyoung Hwa

AU - Kim, Bum Joon

AU - Kim, So Young

AU - Kim, Hee Sun

AU - Kim, Dong Hyun

AU - You, Ho Jin

AU - Hyun, Jin Won

N1 - Funding Information: This research was supported by the study of the DNA repair regulation with disease program and by the program of Basic Atomic Energy Research Institute (BAERI) which is a part of the Nuclear R&D programs grant from the Ministry of Science and Technology of Korea.

PY - 2007

Y1 - 2007

N2 - The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H2O2 treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H2O2 induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.

AB - The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H2O2 treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H2O2 induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.

KW - Cytoprotective properties

KW - Glycitein

KW - Oxidative stress

KW - Reactive oxygen species

UR - https://www.scopus.com/pages/publications/34249824273

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DO - 10.1080/10715760701241618

M3 - Article

C2 - 17516245

AN - SCOPUS:34249824273

SN - 1071-5762

VL - 41

SP - 720

EP - 729

JO - Free Radical Research

JF - Free Radical Research

IS - 6

ER -

Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

Abstract

Bibliographical note

Keywords

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