Fig. 2

Downregulation of NF-κB p65 attenuates neuropathic pain in CCI rats via inhibition of HDAC2. a NF-κB p65 silencing efficiency in microglial cells assessed by Western blot analysis and RT-qPCR. b HDAC2 expression upon PDTC treatment determined by Western blot analysis, normalized to GAPDH. c The luciferase activity of HDAC2 promoter after NF-κB p65 silencing detected by dual-luciferase reporter assay. d, e PWT and PWL in CCI rats intraperitoneally injected with PDTC (50 mg/kg, once a day, for 14 days) (n = 10). f Protein levels of NF-κB p65 and HDAC2 as well as NF-κB p65 phosphorylation extent in spinal dorsal horn in CCI rats determined by Western blot analysis, normalized to GAPDH. *relative to sham-operated rats or microglial cells treated with sh-NC and ^#relative to CCI rats injected with DMSO indicate p < 0.05. All measurement data were expressed as the mean ± standard deviation. Unpaired t test was used to analyze data between the two groups, one-way ANOVA and Tukey’s post hoc test to analyze data among multiple groups, and repeated-measures ANOVA with Bonferroni post hoc test to analyze data at different time points. The cell experiment was repeated three times independently