Fig. 7

Activated STAT3 by binding p300 increased the level of acetylated histone H3 on the Acp5 promoter. A, B Intra-Prl injection of S3I-201 prevented the increases of Acp5 proteins and mRNA induced by the acquisition of comorbid following SNI (n = 3 or 5, unpaired t test, for protein, *p = 0.0134, for mRNA, *p = 0.0124, versus the correspondence vehicle group). C Chromatin immunoprecipitation assay was performed with p-STAT3 antibody following incubation of IL-6 in PC12 cells (n = 3 in each group, unpaired t test, **p = 0.002 versus the vehicle group). D Chromatin immunoprecipitation assay was performed with p-STAT3 antibody in comorbidity rats (n = 3 in each group, unpaired t test, *p = 0.0119 versus the sham group). E The interaction between p-STAT3 and P300 was increased following the acquisition of comorbidity after SNI in rats (n = 4 in each group, unpaired t test, for p-STAT3, *p = 0.0225, for P300, *p = 0.0279, versus the sham group). F The histone acetylation of H3 K9, but not the global histone acetylation of H4, was upregulated on weeks 5 following SNI (n = 4 in each group, unpaired t test, **p = 0.0025 versus the sham group). G Chromatin immunoprecipitation was performed using Ac-H3 antibody on weeks 5 after SNI (n = 3 in each group, unpaired t test, ****p < 0.0001 versus the sham group). H IntraPrL injection of S3I-201 reversed the increased histone acetylation of H3 induced by SNI (n = 4 in each group, unpaired t test, *p = 0.0459 versus the vehicle group). Data are expressed as mean ± SEM