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Original Paper

Melia toosendan Regulates PC12 Cell Differentiation via the Activation of Protein Kinase A and Extracellular Signal-Regulated Kinases

Yu J.C.H.a · Min Z.b · Ip N.Y.a

Author affiliations

aDepartment of Biochemistry, Biotechnology Research Institute and Molecular Neuroscience Center, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, and bDepartment of Natural Medicine Chemistry, China Pharmaceutical University, Nanjing, China

Corresponding Author

Prof. Nancy Y. Ip

Department of Biochemistry Hong Kong University of Science and Technology

Clear Water Bay

Hong Kong (China)

Tel. +852 2358 7304, Fax +852 2358 2765, E-Mail boip@ust.hk

Related Articles for ""

Neurosignals 2004;13:248–257

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Abstract

With a history of several thousand years, traditional Chinese medicine has been well documented to be effective in the treatment of various disorders. We have investigated the activities of potential neuroactive compounds in traditional Chinese medicine such as Melia toosendan using an in vitro model system, rat pheochromocytoma PC12 cells. We report here that treatment of PC12 cells with a crude extract of the fruits of M. toosendan reduces cell growth in a dose-dependent manner without detectable cytotoxicity. Upon treatment with M. toosendan, PC12 cells exhibit robust neurite outgrowth, to a greater extent than that observed with nerve growth factor. Results obtained with specific kinase inhibitors and protein kinase A-deficient PC12 cells indicate that the actions of M. toosendan are mediated by the activation of protein kinase A and extracellular signal-regulated kinases.

© 2004 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 26, 2004
Accepted: March 31, 2004
Published online: August 12, 2004
Issue release date: September – October

Number of Print Pages: 10
Number of Figures: 6
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG


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