Glucagon-like peptide-1 inhibits LPS-induced IL-1β production in cultured rat astrocytes

被引：208

作者：

Iwai, Takashi ^{[1
]}

Ito, Satoshi ^{[1
]}

Tanimitsu, Kahori ^{[1
]}

Udagawa, Shunichi ^{[1
]}

Oka, Jun-Ichiro ^{[1
]}

机构：

[1] Tokyo Univ Sci, Fac Pharmaceut Sci, Pharmacol Lab, Chiba 2788510, Japan

来源：

NEUROSCIENCE RESEARCH | 2006年 / 55卷 / 04期

基金：

日本学术振兴会;

关键词：

glucagon-like peptide-1; interleukin-1; beta; astrocyte; microglia; lipopolysaccharide; cAMP;

D O I：

10.1016/j.neures.2006.04.008

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Glia play an important role in neurotoxicity in neurodegenerative diseases. In this study, we investigated the expression of glucagon-like peptide-1 (GLP-1) and its receptor, and the effects of GLP-1 on lipopolysaccharide (LPS)-induced IL-1 beta mRNA expression and IL-1 beta production in glia. GLP-1-like immunoreactivity was observed in amoeboid microglia, but not ramified microglia or astrocytes. GLP-1 binding and GLP-1 receptor mRNA expression were observed in both astrocytes and microglia. GLP-1-induced morphological changes in microglia from the ramified type to the amoeboid type, suggesting an increase in production and release of endogenous GLP-1. GLP-1 prevented the LPS-induced IL-I beta mRNA expression, which effect was, in turn, inhibited by pretreatment with SQ22536, an adenylate cyclase inhibitor. GLP-1 also increased cAMP concentration and cAMP response element-binding protein phosphorylation in astrocytes. These results suggest that GLP-1 may be a modulator of inflammation in the central nervous system. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

引用

页码：352 / 360

页数：9

共 33 条

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