Fig. 6From: Preemptive intrathecal administration of endomorphins relieves inflammatory pain in male mice via inhibition of p38 MAPK signaling and regulation of inflammatory cytokinesThe involvement of p38 MAPK signal in the preemptive analgesia of endomorphins. a, b Quantitative Western blot analysis of the expression of ERK1/2 and p38 MAPK was performed in ipsilateral DRG tissues. Representative Western blots showed the levels of phosphorylated p38 MAPK or ERK1/2 (top) and total p38 MAPK or ERK1/2 (bottom) in DRG. Lane 1: Control; lane 2: Saline + CFA; lane 3: EM-1 + CFA; lane 4: EM-2 + CFA. Data are presented as the percentage difference relative to the control (n = 5, *P < 0.05 vs. Control, #P < 0.05 vs. Saline). c Repeated administration of the p38 MAPK inhibitor SB203580 (10 and 15 nmol, i.t.) significantly reduced CFA-induced mechanical allodynia (**P < 0.01, ***P < 0.001 vs. Vehicle). d, e Representative photomicrographs of P-p38-immunoreactive neurons (red) in ipsilateral L4 DRG neurons and a graph quantifying the P-p38 expression in the control group, saline-treated CFA group, and endomorphins-treated CFA group were showed. Preemptive intrathecal administration of endomorphins robustly suppressed the increase of P-p38 MAPK immunoreactive neurons as compared with the saline-treated group, and pretreatment with naloxone and β-FNA inhibited the effect of endomorphins. Arrows indicate P-p38 MAPK positive neurons, and triangles indicate the negative neurons (n = 4–6 animals/group, scale bar = 50 μm, ***P < 0.001 vs. Control, ###P < 0.001 vs. Saline, +++P < 0 .001 vs. EM-1 and $$$P < 0.001 vs. EM-2). Data obtained from a, b, and e were statistically analyzed according to one-way ANOVA followed by Bonferroni post-hoc analysis, and data obtained from c were statistically analyzed according to two-way ANOVA followed by Bonferroni post-hoc analysisBack to article page