miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain

Figure 3

MiR-223 could ameliorate neuroinflammation via targeting NLRP3. (a) Schematic representation of the predicted binding sites between miR-223 and NLRP3. (b) Dual-luciferase reporter assays of miR-223 and NLRP3 3′-UTR. The miR-223 mimics or the control (miR-223 NC) was cotransfected with the dual-luciferase vector containing wt or mut pGL3-NLRP3 3′-UTR into BV2 cells and incubated for 48 h. The relative luciferase activity was calculated as the ratio of firefly to Renilla luciferase activity, as measured with the dual-luciferase assay system. compared to the miR-223 NC group. (c) Western blot detecting the expression of NLRP3, ASC, and activated caspase-1 in the spinal cords of CCI model mice infected with Lenti-vector or with Lenti-miR-223. (d) Quantification of NLRP3, ASC, and caspase-1 expression levels; data were normalized by β-actin. n = 6. compared to the sham group. compared to the CCI group. (e) Representative picture showing the Western blot analysis for IL-1β and IL-18. (f) The intensity of each protein was normalized to the signal intensity of the corresponding pro-IL-1β or pro-IL-18. n = 6. compared to the sham group. compared to the CCI group.

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