Interleukin-Ira inhibits Fos expression and hyperalgesia in rats

被引：7

作者：

Li, Aihui

Lao, Lixing

Wang, Yi

Zhang, Haiqing

Ren, Ke

Berman, Brian M.

Zhang, Ruixin

机构：

[1] Univ Maryland, Sch Med, Ctr Integrat Med, Baltimore, MD 21201 USA

[2] Univ Maryland, Dent Sch, Dept Biomed Sci, Baltimore, MD 21201 USA

来源：

NEUROREPORT | 2007年 / 18卷 / 05期

关键词：

Fos; hyperalgesia; interleukin-I beta; interleukin-Ira; intrathecal; rats; spinal cord;

D O I：

10.1097/WNR.0b013e3280586839

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

It is known that interleukin-1 beta facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1 beta in the expression of Fos, a marker of neuronal activation, and hyperalgesia caused by injecting complete Freund's adjuvant into one hind paw of the rat. Interleukin-receptor antagonist (interleukin-Ira, 0.005 mg/rat) was given intrathecally twice, 24 h before complete Freund's adjuvant and immediately before complete Freund's adjuvant injection, to block interleukin-1 beta action. Fos expression was measured 2 h after complete Freund's adjuvant injection. Paw withdrawal latency was used to assess hyperalgesia. The findings were that interleukin-Ira inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1 beta facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression.

引用

页码：495 / 498

页数：4

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