董悦生

个人信息Personal Information

副教授

博士生导师

硕士生导师

性别:男

毕业院校:中国协和医科大学

学位:博士

所在单位:生物工程学院

学科:生物化工. 微生物学. 微生物与生化药学

办公地点:辽宁省大连市高新园区凌工路2号大连理工大学西部校区生物工程学院309室

联系方式:辽宁省大连市高新园区凌工路2号大连理工大学生物工程学院

电子邮箱:yshdong@dlut.edu.cn

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Catalpol attenuates nitric oxide increase via ERK signaling pathways induced by rotenone in mesencephalic neurons

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论文类型:期刊论文

发表时间:2009-03-01

发表刊物:NEUROCHEMISTRY INTERNATIONAL

收录刊物:SCIE、PubMed、Scopus

卷号:54

期号:3-4

页面范围:264-270

ISSN号:0197-0186

关键字:Rotenone; Catalpol; Mesencephalic neurons; NO; iNOS; ERK

摘要:Catalpol has been shown to rescue neurons from kinds of damage in vitro and in vivo in previous reports. However, the effect of catalpol on the nitric oxide (NO) system via MAPKs signaling pathway of mesencephalic neurons largely remains to be verified. The current study examined that whether catalpol modulated NO and iNOS increase by rotenone in primary mesencephalic neurons and investigated its underlying signaling pathways. Present results indicated that catalpol inhibited primary mesencephalic neurons from apoptosis by morphological assay, immunocytochemistry and flow cytometric evaluation. Moreover, the ERK signaling pathway plays an important role in NO-mediated degeneration of neuron. The current results suggest that catalpol is a potential agent for the prevention of neurons apoptosis by regulating NO and iNOS increase in ERK-mediated neurodegenerative disorders. (C) 2008 Elsevier Ltd. All rights reserved.