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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: NF-κB p65-dependent transcriptional regulation of histone deacetylase 2 contributes to the chronic constriction injury-induced neuropathic pain via the microRNA-183/TXNIP/NLRP3 axis

Fig. 3

Downregulation of HDAC2 leads to elevated miR-183 expression and attenuates neuropathic pain in CCI rats. a HDAC2 silencing efficiency in microglial cells determined by Western blot analysis, normalized to GAPDH. b miR-183 expression in microglial cells treated with sh-HDAC2 determined by RT-qPCR, normalized to U6. c Enrichment of HDAC2 in the miR-183 promoter region detected by ChIP-qPCR assay. d Effect of HDAC2 silencing on histone acetylated H4 in miR-183 promoter detected by ChIP-qPCR assay. e, f PWT and PWL of CCI rats injected with SAHA (20 mg/kg, once a day) and lentivirus-transduced sh-HDAC2 (n = 10). g miR-183 expression in spinal dorsal horn of CCI rats injected with SAHA and lentivirus-transduced sh-HDAC2 determined by RT-qPCR, normalized to U6 (n = 10). *relative to sham-operated rats, microglial cells treated with sh-NC, or IgG, #relative to CCI rats, and $relative to CCI rats injected with sh-NC 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 and Bonferroni post hoc test to analyze data at different time points. The cell experiment was repeated three times independently

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