Fig. 5

Overexpression of miR-183 inhibits inflammation in CCI rats via the downregulation of the TXNIP-NLRP3 axis. a NLRP3 protein expression in the spinal cord of CCI rats determined using Western blot analysis, normalized to GAPDH (n = 10). b Expression of NLRP3 in Iba-1-labeled microglial cells of CCI rat spinal cord detected by immunofluorescence staining (n = 5) (scale bar = 50 μm). c NLRP3 protein expression in microglial cells treated with exogenous miR-183 mimicdetermined using Western blot analysis, normalized to GAPDH (n = 3). d Binding relationship between TXNIP and NLRP3 detected by Co-IP assay. e Protein expression of NLRP3, ASC, and caspase-1 in microglial cells after forced expression miR-183 and TXNIP measured using Western blot analysis, normalized to GAPDH. f Expression of IL-1β in microglial cells after forced expression miR-183 and TXNIP measured using ELISA (n = 10). g Expression of NLRP3, ASC, and caspase-1 in spinal cord of CCI rats injected with lentivirus expressing miR-183 agomir or in combination with oe-TXNIP measured using Western blot analysis, normalized to GAPDH. h Expression of IL-1β in spinal cord of CCI rats injected with lentivirus expressing miR-183 agomir or in combination with oe-TXNIP measured using ELISA (n = 10). *relative to sham-operated rats, microglial cells treated with mimic NC and ^#relative to microglial cells treated with miR-183 mimic or CCI rats injected with miR-183 agomir indicate p < 0.05. All measurement data were expressed as 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