Fig. 8

Peripheral adipoR1 participated in mechanical pain hypersensitivity. A Escape threshold after intra-TG injection of vehicle or adiponectin at 0.1 nmol, 1 nmol or 5 nmol. *p < 0.05 (vs. vehicle) at the corresponding time point, two-way ANOVA. B, C Administration of adipoR1-siRNA (B) or PKCβ1-siRNA (C) prevented adiponectin-induced mechanical hypersensitivity. *p < 0.05 (vs. vehicle); ^#p < 0.05 (vs. APN) in NC-siRNA-treated groups, two-way ANOVA. D Pretreatment with TTA-P2 (1 nmol) or Z941 (0.5 nmol) attenuated adiponectin (1 nmol)-induced mechanical hypersensitivity. *p < 0.05 (vs. vehicle), ^#p < 0.05 (vs. APN) at the 1-h time point, two-way ANOVA. E Escape threshold to mechanical stimuli in the sham- or CCI-ION-operated groups. ***p < 0.01 (vs. sham) at the corresponding time point, two-way ANOVA. F Protein abundance of adipoR1 in TGs 14 days following CCI-ION or sham surgery. *p < 0.05 (vs. sham), unpaired t test. Representative blots of at least 3 independent experiments are shown. G Intra-TG administration of adipoR1-siRNA 14 days after CCI-ION significantly attenuated mechanical hypersensitivity in CCI-ION mice. *p < 0.05 and **p < 0.01 (vs. NC-siRNA), two-way ANOVA. H Effect of Cav3.2-siRNA vs. NC-siRNA (Day 0) on adipoR1-siRNA (intra-TG injection on Day 3)-induced alleviation of mechanical allodynia in CCI-ION mice. Intra-TG injection of adipoR1-siRNA did not have additive effects to Cav3.2-siRNA on mechanical allodynia in CCI-ION mice. ** p < 0.01 (vs. CCI-ION) at -14 days, ^# p < 0.05 and ^## p < 0.01 (vs. NC-siRNA) at the 3-day point in CCI-ION mice, ⁺ p < 0.05 (vs. Cav3.2-siRNA) at the 0-day point in CCI-ION mice, two-way ANOVA