Protective effects of catalpol against H2O2-induced oxidative stress in astrocytes primary cultures

被引:92
作者
Bi, Jing [1 ]
Jiang, Bo [1 ]
Liu, Jian Hui [2 ]
Lei, Chen [3 ]
Zhang, Xiu Li [1 ]
An, Li-Jia [1 ]
机构
[1] Dalian Univ Technol, Sch Environm & Biol Sci & Technol, Dalian 116024, Liaoning, Peoples R China
[2] Res Ctr Pharmaceut Chem & Chem Biol, Chongqing 400067, Peoples R China
[3] Third Hosp Xiamen, CT Dept, Xiamen 361100, Peoples R China
关键词
catalpol; oxidative stress; neuroprotection; astrocyte; H2O2; cytotoxicity;
D O I
10.1016/j.neulet.2008.07.029
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It has been proposed that ROS production, including H2O2, may lead to neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Catalpol, an iridoid glycoside, presents in the root of Rehmannia glutinosa, protects cells and mice from damage caused by a variety of toxic stimuli. In this study, we investigated whether catalpol could protect astrocytes from oxidant stress induced by H2O2 because of the critical role of astrocytes in the brain and found the possible mechanism of protection. The results showed that catalpol could significantly increase the cell viability and reduce the intracellular ROS formation. Furthermore, catalpol attenuated H2O2-induced oxidative stress via preventing the decrease in the activities of antioxidant enzymes in glutathione redox cycling such as glutathione peroxidase, glutathione reductase and glutathione content. However, the catalase activity did not appear to be elevated by catalpol adequately. Together, the main mechanism underlying the protective effects of catalpol in H2O2-injured astrocytes might be related to the maintenance of glutathione metabolism balance and the decrease of ROS formation. Therefore, catalpol may be developed as a potential preventive or therapeutic drug for neurodegenerative diseases associated with oxidative stress. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:224 / 227
页数:4
相关论文
共 24 条
[1]   OXIDANTS, ANTIOXIDANTS, AND THE DEGENERATIVE DISEASES OF AGING [J].
AMES, BN ;
SHIGENAGA, MK ;
HAGEN, TM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7915-7922
[2]   The free radical theory of aging matures [J].
Beckman, KB ;
Ames, BN .
PHYSIOLOGICAL REVIEWS, 1998, 78 (02) :547-581
[3]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[4]   Metabolism and functions of glutathione in brain [J].
Dringen, R .
PROGRESS IN NEUROBIOLOGY, 2000, 62 (06) :649-671
[5]   Glutathione restoration as indicator for cellular metabolism of astroglial cells [J].
Dringen, R ;
Hamprecht, B .
DEVELOPMENTAL NEUROSCIENCE, 1998, 20 (4-5) :401-407
[6]   Peroxide detoxification by brain cells [J].
Dringen, R ;
Pawlowski, PG ;
Hirrlinger, J .
JOURNAL OF NEUROSCIENCE RESEARCH, 2005, 79 (1-2) :157-165
[7]   Involvement of glutathione peroxidase and catalase in the disposal of exogenous hydrogen peroxide by cultured astroglial cells [J].
Dringen, R ;
Hamprecht, B .
BRAIN RESEARCH, 1997, 759 (01) :67-75
[8]   Roles of mitochondria in health and disease [J].
Duchen, MR .
DIABETES, 2004, 53 :S96-S102
[9]  
GLENDA MB, 2007, FREE RADIC BIOL MED, V42, P1222
[10]  
Gutteridge JMC, 2000, ANN NY ACAD SCI, V899, P136, DOI 10.1111/j.1749-6632.2000.tb06182.x