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Downregulation of inducible nitric oxide synthetase by neurotrophin-3 in microglia

✍ Scribed by Shun-Fen Tzeng; Hsin-Ying Huang

Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
234 KB
Volume
90
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

Microglia activated after many neurological degeneration of the central nervous system (CNS) act as important regulators for neuropathogenesis in the injured CNS via producing proinflammatory mediators, such as nitric oxide (NO), TNF‐α, and IL‐1β. Neurotrophin‐3 (NT‐3) is a well‐known trophic factor for neural survival, development, and plasticity. Activated microglia are NT‐3‐producing cells in the injured CNS, and express its receptor‐TrkC. However, little is known about the effect of NT‐3 on activated microglia. In this study, pre‐treatment of a mouse microglial cell line, BV2, with NT‐3 for 24 h indicated that NT‐3 reduced the inducible form of NO synthase (iNOS), NO, and TNF‐α in BV2 stimulated with lipopolysaccharide (LPS). NT‐3 exerted less effect on the reduction of these proinflammatory mediators when it was added to BV2 cultures either simultaneously with LPS or post LPS treatment. These findings indicate that NT‐3 may serve as an anti‐inflammatory factor to suppress microglial activation. J. Cell. Biochem. 90: 227–233, 2003. © 2003 Wiley‐Liss, Inc.

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