Fig. 7.
Nuclear factor-κB (NF-κB) p65 activity is required for the increased acetylation of histone H4 on the cx3cl1 promoter region induced by paclitaxel (Pacl). (A) Treatment with paclitaxel significantly increased the global acetylation of histone H4, but not H3 K9, in the spinal dorsal horn. n = 6 in each group; **P < 0.01 vs. corresponding control group (Con). (B) Chromatin immunoprecipitation (ChIP) assay were performed with or without acetylated H4 antibody. Increased acetylation of histone H4 on the cx3cl1 promoter region flanking NF-κB p65-binding site was reduced by ammonium pyrrolidinedithiocarbamate (PDTC) or p65 small interfering RNA (siRNA) in rats receiving paclitaxel treatment. n = 7 in each group; **P < 0.01 vs. corresponding control group, ##P < 0.01 vs. corresponding paclitaxel group. No Ab = normal immunoglobulin G without specific antibody.

Nuclear factor-κB (NF-κB) p65 activity is required for the increased acetylation of histone H4 on the cx3cl1 promoter region induced by paclitaxel (Pacl). (A) Treatment with paclitaxel significantly increased the global acetylation of histone H4, but not H3 K9, in the spinal dorsal horn. n = 6 in each group; **P < 0.01 vs. corresponding control group (Con). (B) Chromatin immunoprecipitation (ChIP) assay were performed with or without acetylated H4 antibody. Increased acetylation of histone H4 on the cx3cl1 promoter region flanking NF-κB p65-binding site was reduced by ammonium pyrrolidinedithiocarbamate (PDTC) or p65 small interfering RNA (siRNA) in rats receiving paclitaxel treatment. n = 7 in each group; **P < 0.01 vs. corresponding control group, ##P < 0.01 vs. corresponding paclitaxel group. No Ab = normal immunoglobulin G without specific antibody.

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