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论文类型：期刊论文

发表时间：2008-09-19

发表刊物：NEUROSCIENCE LETTERS

收录刊物：SCIE、PubMed、Scopus

卷号：442

期号：3

页面范围：224-227

ISSN号：0304-3940

关键字：catalpol; oxidative stress; neuroprotection; astrocyte; H2O2 cytotoxicity

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.