Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride

被引:59
作者
Tan, Chu-Bing [1 ,2 ,3 ]
Gao, Mei [1 ,2 ]
Xu, Wei-Ren [3 ]
Yang, Xiu-Ying [1 ,2 ]
Zhu, Xiao-Ming [1 ,2 ]
Du, Guan-Hua [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Inst Mat Med, Beijing 100050, Peoples R China
[2] Peking Union Med Coll, Beijing 100050, Peoples R China
[3] Tianjin Inst Pharmaceut Res, Tianjin Key Lab Mol Design & Drug Discovery, Tianjin 300193, Peoples R China
关键词
salidroside; cobalt chloride; apoptosis; endothelial cell; PC12; CELLS; PROTEIN-KINASE; HELA-CELLS; ACTIVATION; HYPOXIA; INHIBITION; MECHANISMS; DEATH;
D O I
10.1248/bpb.32.1359
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Salidroside is a major constituent of Rhodiola rosea L. that elicits beneficial effects for ischemic cardiovascular diseases. The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimic king agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases.
引用
收藏
页码:1359 / 1363
页数:5
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