Fig. 6

Chronic treatment with IL-1ra (IL-1β antagonist) reversed NTG-induced hyperalgesia. a Drug administered in the third experiment. In treatment groups, mice were treated with VEH or IL-1ra (4 μg/mouse, I.C.V.) daily for 11 days. On days 3, 5, 7, 9 and 11, basal threshold responses were determined, and then mice were injected with VEH or IL-1ra. 30–45 min later, mice were injected with nitroglycerin (NTG; 10 mg/kg, i.p.). Acute treatment responses were assessed 2 h following NTG administration. The saline group and NTG group just were injected saline or NTG, respectively, and the mechanical sensitivity responses were also tested before injection and 2 h after injection. b, c Basal threshold responses were significantly decreased after NTG administrations. ***p < 0.001 for the saline group compared to the NTG group. In the group receiving IL-1ra-preventative treatment, basal threshold responses induced by NTG significantly reversed. ^###p < 0.001 for the IL-1ra+NTG group compared to the NTG group. Two-way RM ANOVA and Holm-Sidak post hoc analysis (n = 8 mice per group). d, e NTG injection induced acute hyperalgesia. ***p < 0.001 for the saline group compared to the NTG group. Acute NTG-induced hyperalgesia were blocked by treatment with IL-1ra. ^###p < 0.001 for the IL-1ra+NTG group compared to the NTG group. Two-way RM ANOVA and Holm-Sidak post hoc analysis (n = 8 mice per group). I.C.V., intracerebroventricular