Quercetin protects the hydrogen peroxide-induced apoptosis via inhibition of mitochondrial dysfuntion in H9c2 cardiomyoblast cells

被引:111
作者
Park, C
So, HS
Shin, CH
Baek, SH
Moon, BS
Shin, SH
Lee, HS
Lee, DW
Park, R [1 ]
机构
[1] Wonkwang Univ, Sch Med, Dept Microbiol, Iksan 570749, Jeonbuk, South Korea
[2] Wonkwang Univ, Profess Grad Sch Oriental Med, Iksan 570749, Jeonbuk, South Korea
[3] Chonbuk Natl Univ, Sch Med, Dept Ophthalmol, Jeonjy, South Korea
[4] SKY Sports Med Lab, Seoul, South Korea
关键词
quercetin; oxidative stress; mitochondrial dysfunction; caspase cascade;
D O I
10.1016/S0006-2952(03)00478-7
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Quercetin possesses a broad range of pharmacological properties, including protection of LDL from oxidation. However, little is known about the mechanism by which quercetin rescues cardiomyoblasts from oxidative damage. This study was designed to investigate the protective mechanism of quercetin on H2O2-induced toxicity of H9c2 cardiomyoblasts. Oxidative stress, such as H2O2, ZnCl2, and menadione, significantly decreased the viability of H9c2 cells, which was accompanied with apparent apoptotic features, including fragmentation of genomic DNA as well as activation of caspase protease. However, quercetin markedly inhibited the apoptotic characteristics via reduction of intracellular reactive oxygen species generation. Also, it prevented the H2O2-mediated mitochondrial dysfunction, including disruption of mitochondria membrane permeability transition as well as an increase in expression of apoptogenic Bcl-2 proteins, Bcl-2 and Bcl-X-L. Furthermore, pretreatment of quercetin inhibited the activation of caspase-3, thereby both cleavage of poly(ADP-ribose) polymerase and degradation of inhibitor of caspase-activated DNase/DNA fragmentation factor by H2O2 were completely abolished. Taken together, these data suggest that protective effects of quercetin against oxidative injuries of H9c2 cardiomyoblasts may be achieved via modulation of mitochondrial dysfunction and inhibition of caspase activity. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:1287 / 1295
页数:9
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