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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Preemptive intrathecal administration of endomorphins relieves inflammatory pain in male mice via inhibition of p38 MAPK signaling and regulation of inflammatory cytokines

Fig. 6

The 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 analysis

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