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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: TNF-α/STAT3 pathway epigenetically upregulates Nav1.6 expression in DRG and contributes to neuropathic pain induced by L5-VRT

Fig. 5

TNF-α via activating STAT3 enhanced the binding of p-STAT3 in the Scn8a promoter in DRG. a Chromatin immunoprecipitation assay showed the binding of p-STAT3 in the Scn8a promoter after L5-VRT. n = 6 per group, **P < 0.01 versus the sham group, ##P < 0.01 versus the corresponding L5-VRT group. b Increased p-STAT3 content was significantly immunoprecipitated by the p300 antibody, and increased p300 was also significantly immunoprecipitated by the p-STAT3 antibody on the different time points after L5-VRT. n = 5 per group, **P < 0.01 versus the sham group. c Representative blots and histogram showed the expression of acetylated histone H3 following L5-VRT. n = 5 per group. d Representative blots and histogram showed the expression of acetylated histone H4 after L5-VRT. n = 5 per group, **P < 0.01 versus the sham group. e Acetylation of H4 on the promoter region of Scn8a the flanking STAT3 binding site in chromatin immunoprecipitation assay in rats with S3I-201 treatment. n = 6 per group, **P < 0.01 versus the sham group, ##P < 0.01 versus the corresponding VRT group. f The change of histone H4 acetylation on the promoter region of Scn8a flanking the STAT3 binding site in the STAT3flox/flox mice which were injected with AAV-Cre-GFP. n = 6 per group, **P < 0.01 versus the sham group, ##P < 0.01 versus the corresponding VRT group. g The effect of thalidomide (i.p.) on the histone H4 acetylation on the Scn8a promoter region following L5-VRT. n = 6 per group, **P < 0.01 versus the sham group, ##P < 0.01 versus the corresponding VRT group

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