4.5 Article

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

期刊

NEUROCHEMISTRY INTERNATIONAL
卷 54, 期 3-4, 页码 264-270

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2008.12.003

关键词

Rotenone; Catalpol; Mesencephalic neurons; NO; iNOS; ERK

资金

  1. Key Fund of International Cooperation [2005DFA40790]
  2. Natural Science Foundation of Liaoning [20072185]

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据