姜波

个人信息Personal Information

副教授

硕士生导师

性别:女

毕业院校:大连理工大学

学位:博士

所在单位:生物工程学院

学科:生物化工. 药理学. 神经生物学

办公地点:生物工程学院 323

联系方式:bojiang@dlut.edu.cn 13842650392

电子邮箱:bojiang@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.