Figure 3

Inhibition of NF- κ B signaling attenuated pain behavior in the rats with bone cancer. (A) Implantation of tumor cells in the tibias significantly increased the phosphorylation of NF-κB subunit p65 (t = 2.93, P = 0.01), but not the total p65 (t = 0.54, P > 0.05), in the spinal dorsal horn of the rats (n = 7 rats in each group); (B) Blockade of NF-κB signaling by PDTC (1 μg, from day 3 through day 15) significantly attenuated the upregulation of spinal BDNF in the rats with bone cancer-induced pain (t = 3.49, P < 0.01), while no change was observed in the control rats (t = 0.15, P > 0.05; n = 8–9 rats per group); (C) Intrathecal injection of PDTC significantly attenuated the increase of input (stimuli intensity) – output (EPSC amplitude) response in the dorsal horn neurons in the modeled rats (F_{(1, 19)} = 9.76, P < 0.01; n = 9–12 neurons per group); (D) Intrathecal injection of PDTC significantly recovered the ipsilateral paw withdrawal threshold response to mechanical (F_{(1, 17)} = 11.63, P < 0.01) and radiant thermal stimuli (F_{(1, 17)} = 9.81, P < 0.01) in the rats with bone cancer (n = 9–10 rats per group). Control vs. TCI: *, P < 0.05; **, P < 0.01; TCI vs. TCI + PDTC: ♦, P < 0.05; ♦♦, P < 0.01.