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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Reduction of SIRT1 epigenetically upregulates NALP1 expression and contributes to neuropathic pain induced by chemotherapeutic drug bortezomib

Fig. 5

Activated STAT3 by binding p300 increased the level of acetylated histone H3and H4 on the Nalp1 promoter. Continuous injection of STAT3 activity inhibitor S3I-201 (100 μg/10 μl for 10 days, i.t.) inhibited the upregulation of NALP1 mRNA (a) and protein (b) level on day 10 following BTZ treatment. n = 8 in each group, **P < 0.01 versus the vehicle group, ##P < 0.01 versus the corresponding BTZ group. c A marked green fluoresces in the dorsal horn of mice was observed on day 21 after AAV8-Cre-GFP injection. d Local deficiency of STAT3 by intrathecal injection of AAV-Cre-GFP in STAT3flox/flox mice significantly reduced the upregulation of NALP1 protein in spinal dorsal horn induced by BTZ treatment. n = 6 in each group, **P < 0.01 versus vehicle group, ##P < 0.01 versus the corresponding AAV-GFP group. e Increased p300 was significantly immunoprecipitated with p-STAT3 antibody in spinal dorsal horn of rats following BTZ administration. n = 6 in each group, **P < 0.01 versus vehicle group. f Increased p-STAT3 was significantly immunoprecipitated with P300 antibody on the different time points after bortezomib treatment. n = 6 in each group, **P < 0.01 versus vehicle group. g Intrathecal application of S3I-201 reduced the increase of acetylated H3 or H4 on Nalp1 gene promoter region containing p-STAT3-binding site on day 10 following BTZ treatment. n = 6 in each group, **P < 0.01 versus vehicle group, ##P < 0.01 versus the corresponding BTZ group. h Local deficiency of STAT3 by intrathecal injection of AAV-Cre-GFP into STAT3flox/flox mice decreased the upregulation of H3 or H4 acetylation on Nalp1 gene promoter induced by BTZ. n = 6 in each group, **P < 0.01 versus vehicle group, ##P < 0.01 versus the corresponding AAV-GFP injected BTZ group

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