Rb1 Protects Endothelial Cells from Hydrogen Peroxide-Induced Cell Senescence by Modulating Redox Status

被引:29
作者
Liu, Ding-Hui [1 ]
Chen, Yan-Ming [2 ]
Liu, Yong [1 ]
Hao, Bao-Shun [1 ]
Zhou, Bin [1 ]
Wu, Lin [1 ]
Wang, Min [1 ]
Chen, Lin [1 ]
Wu, Wei-Kang [3 ]
Qian, Xiao-Xian [1 ,3 ]
机构
[1] Sun Yat Sen Univ, Dept Cardiol, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Dept Endocrinol, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China
[3] Sun Yat Sen Univ, Inst Integrated Tradit Chinese & Western Med, Guangzhou 510630, Guangdong, Peoples R China
关键词
senescence; human umbilical vein endothelial cell; reactive oxygen species; antioxidant; GINSENOSIDE RB1; SUPEROXIDE-DISMUTASE; EXPRESSION; EVOLUTION; DAMAGE;
D O I
10.1248/bpb.34.1072
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Senescence of endothelial cells has been proposed to play an important role in endothelial dysfunction and atherogenesis. In the present study we aimed to investigate whether ginsenoside Rb1, a major constituent of ginseng, protects endothelial cells from H2O2-induced endothelial senescence. While H2O2 induced premature senescent-like phenotype of human umbilical vein endothelial cells (HUVECs), as judged by increased senescence-associated beta-galactosidase (SA-beta-gal) activity, enlarged, flattened cell morphology and sustained growth arrest, our results demonstrated that Rb1 protected endothelial cells from oxidative stress induced senescence. Mechanistically, we found that Rb1 could markedly increase intracellular superoxide dismutase (Cu/Zn SOD/SOD1) activity and decrease the malondialdehyde (MDA) level in H2O2-treated HUVECs, and suppress the generation of intracellular reactive oxygen species (ROS). Consistent with these findings, Rb1 could effectively restore the protein expression of Cu/Zn SOD, which was down-regulated in H2O2 treated cells. Taken together, our data demonstrate that Rb1 exhibits antioxidant effects and antagonizes H2O2-induced cellular senescence.
引用
收藏
页码:1072 / 1077
页数:6
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