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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Pain. 2014 Sep 19;155(12):2560–2567. doi: 10.1016/j.pain.2014.09.016

Fig. 2. IB-MECA prevents activation of NFκB and MAPKs in the spinal cord during paclitaxel-induced neuropathic pain.

Fig. 2

When compared to vehicle (V, open bars), administration of paclitaxel (P, black bars) increased IκBα degradation (A), cytosolic phosphorylation of NFκB p65 (B), nuclear translocation of NFκB p65 (C), and phosphorylation of ERK1/2 (D) and p38 (E). These paclitaxel-induced events were blocked by daily administration of IB-MECA (D0–15, 0.1 mg/kg/d; gray bars, A–E). Representative blots are shown. Results are expressed as mean ± SD for n=5–6 rats and analyzed by one-way ANOVA with Dunnett’s comparisons. *P<0.05 vs. Vehicle; †P<0.05 vs. Paclitaxel