Myricetin suppresses oxidative stress-induced cell damage via both direct and indirect antioxidant action

被引:87
作者
Wang, Zhi Hong [1 ]
Kang, Kyoung Ah [1 ]
Zhang, Rui [1 ]
Piao, Mei Jing [1 ]
Jo, Su Hyun [2 ]
Kim, Ju Sun [3 ,4 ]
Kang, Sam Sik [3 ,4 ]
Lee, Jong Sung [5 ]
Park, Deok Hoon [5 ]
Hyun, Jin Won [1 ]
机构
[1] Jeju Natl Univ, Sch Med, Jeju Si 690756, South Korea
[2] Kangwon Natl Univ, Coll Med, Dept Physiol, Inst Biosci & Biotechnol, Chunchon 200701, South Korea
[3] Seoul Natl Univ, Inst Nat Prod Res, Seoul 110460, South Korea
[4] Seoul Natl Univ, Coll Pharm, Seoul 110460, South Korea
[5] Biospectrum Life Sci Inst, Gunpo 435833, South Korea
关键词
Myricetin; Reactive oxygen species; Antioxidant enzyme; Lipid peroxidation; DNA strand breakage; GENTAMICIN-INDUCED NEPHROTOXICITY; RADICAL SCAVENGING ACTIVITY; SUPEROXIDE-DISMUTASE; LIPID-PEROXIDATION; INDUCED APOPTOSIS; IRON CHELATION; STRAND BREAKS; FLAVONOIDS; INFLAMMATION; ASSAY;
D O I
10.1016/j.etap.2009.08.007
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
We evaluated the cytoprotective effect of myricetin on oxidative stress damaged cells by assessment of the scavenging effect of reactive oxygen species(ROS)and the activities of antioxidant enzymes. Myricetin showed the scavenging effect of 1,1 -diphenyl-2-picrylhydrazyl (DPPH) radicals on intracellular ROS. In addition, myricetin restored the activity and protein expression of cellular antioxidant defense enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) reduced by hydrogen peroxide (H2O2) treatment. H2O2-induced cellular DNA and lipid damages, and myricetin was found to prevent the DNA damage shown by inhibition of DNA tail and it decreased nuclear phospho-histone H2A.X expression, which are both markers for DNA strand breakage. Membrane lipid peroxidation was also attenuated as shown by inhibition of TBARS formation and of fluorescence intensity of diphenyl-1-pyrenylphosphine (DPPP). These results suggest that myricetin protects cells against H2O2-induced cell damage via inhibition of ROS generation and activation of antioxidant enzymes. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:12 / 18
页数:7
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