Download original image
Fig. 9. Rats were treated with colchicine (COL, 10 mmol/L) in the sciatic nerve, and (or) botulinum toxin type A (BTX-A, 10 U/kg) injected to the plantar surface of the hind paw. The levels of CXCL13, CXCR5, and GAT-1 were increased in the spinal cord, DRG, sciatic nerve and hind paw of chronic constriction injury (CCI) rats. Both COL and BTX-A attenuated these increases. But in the spinal cord (A, E, I, M) and DRG (B, F, J, N), combination of COL and BTX-A could partly reversed BTX-A-induced CXCL13, CXCR5, and GAT-1 inhibition. The effect of combination of COL and BTX-A on the BTX-A-induced inhibition of GAT-1 in sciatic nerve (O) and CXCR5 in hind paw (L) was not significant. The trends of the expression of CXCL13 in sciatic nerve (C, G) and hind paw (D, H), CXCR5 in sciatic nerve (K), and GAT-1 in hind paw (P) were similar with those in spinal cord and DRG. These suggest that blocking axonal transport by COL can reverse BTX-A-induced inhibition neuro-inflammation. The error bar means mean ± standard deviation. CXCL13: chemokine ligand 13, CXCR5: C-X-C chemokine receptor type 5, GAT-1: GABA transporter 1, DRG: dorsal root ganglia, NS: normal saline. aP < 0.05 vs. the sham group, bP < 0.05 vs. the CCI-NS-NS group, cP < 0.05 vs. CCI-COL-NS group, One-way ANOVA, n = 3 in each group.
Korean J Pain 2022;35:391~402
© Korean J Pain