Fig. 7.
The effect of intervening CXCL1/CXCR2 signaling on morphine tolerance. All the drugs were administered intrathecally using an osmotic pump. The infusion rate was as follows: morphine 15 μg/h, CXCL1 1.2 ng/h, CXCL1-Ab 3.6 ng/h, antileukinate hexapeptide (CXCR2 receptor blocker) 5 μg/h. Note that exogenous CXCL1 markedly accelerated the development of morphine tolerance (A), whereas CXCL1 neutralizing antibody (A) or antileukinate hexapeptide (B) inhibited the induction of morphine tolerance and partially restored morphine analgesic efficacy. *P < 0.05 as compared with morphine group at different time points tested by Bonferroni correction.