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Updated: Jul 15, 2026

Development of Recombinant Proteins to Treat Chronic Pain
Published on: April 11, 2018
Interleukin-1ra inhibits Fos expression and hyperalgesia in rats
Aihui Li1, Lixing Lao, Yi Wang
1Center for Integrative Medicine, School of Medicine, Department of Biomedical Sciences, University of Maryland, Baltimore, Maryland 21201, USA.
Abstract:
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.