Interleukin-1ra inhibits Fos expression and hyperalgesia in rats.
It is known that interleukin-1beta facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1beta 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-1ra, 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-1beta 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-1ra inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1beta facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression.
Li
Aihui
A
Center for Integrative Medicine, School of Medicine, Department of Biomedical Sciences, University of Maryland, Baltimore, Maryland 21201, USA.
Lao
Lixing
L
Wang
Yi
Y
Zhang
Haiqing
H
Ren
Ke
K
Berman
Brian M
BM
Zhang
Ruixin
R
D000818:Animals; D005620:Freund's Adjuvant; D007839:Functional Laterality / Q000502:physiology; D005786:Gene Expression Regulation / Q000187:drug effects*; D006930:Hyperalgesia / Q000139:chemically induced / Q000517:prevention & control*; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use*; D008297:Male; D010147:Pain Measurement / Q000379:methods; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D053590:Interleukin 1 Receptor Antagonist Protein; D016760:Proto-Oncogene Proteins c-fos; D005620:Freund's Adjuvant