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Fig. 5 | Molecular Medicine

Fig. 5

From: AAV-glycine receptor α3 alleviates CFA-induced inflammatory pain by downregulating ERK phosphorylation and proinflammatory cytokine expression in SD rats

Fig. 5

Effects of AAV-GlyRα3 on ERK and p38 phosphorylation in CFA‑treated rats. Intrathecal NaCl, AAV (2.5 × 1012 vg), or AAV-GlyRα3 (2.5 × 1012 vg) injection 8 weeks later CFA (100 μg/100 μl) was given through hind paw injection. After 2 days of CFA treatment, L5 DRGs were collected to evaluate ERK and p38 phosphorylation. By A immunofluorescence, B western blotting and quantification, a magnification image showing the induction of ERK phosphorylation in the GNF and GVF groups. CFA induces sustained activation of ERK, which was repressed in the Gα3F group. Double immunofluorescence labeling of C p-ERK with NeuN and D p-ERK with GFAP indicated colocalization of p-ERK with NeuN in neurons and satellite glial cell in the DRG. E Immunofluorescence imaging revealed p38 phosphorylation in the GNF, GVF and Gα3F groups. Double immunofluorescence labeling of F p-p38 with NeuN and G p-p38 with NF200 revealed p-p38 expression in small neurons. The data represent the means ± SE (n = 6–9 per group). One-way ANOVA. *p < 0.05, **p < 0.01, ***p < 0.001. Scale bars: 50–100 μm

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