Skip to main content
. 2019 Apr 18;12:1287–1296. doi: 10.2147/JPR.S197168

Figure 4.

Figure 4

NF-κB participates in the neuropathic pain regulation of TRPM8 in DRGs of chronic constriction injury (CCI) rats. To exam whether NF-κB involved in the pain regulation of TRPM8, NF-κB p65 expression (A and B) and pain thresholds (C and D) were detected in Sham, CCI rats and CCI rats with TRPM8 blockade (with AMTB) or TRPM8+NF-κB blockade (with PDTC). (A and B) Western blotting images and statistics of NF-κB expression levels. Data are expressed as mean±SD, n=3. *P<0.05 vs Sham group, #P<0.05 vs CCI group (C and D). Pain behavior tests showed that compared with the CCI group, NF-κB blockade with PDTC significantly decreased the paw lift times and reduced thermal hyperalgesia. When the TRPM8 and NF-κB were both blocked, the paw lift times on cold plate decreased more on the 3rd, 7th, 10th and 14th day in CCI rats compared with that of NF-κB blockade CCI rats, but no difference of thermal hyperalgesia was found between NF-κB inhibition group and NF-κB + AMTB blockade group at the time points. Data are expressed as mean±SD, n=12. *P<0.05 vs NF-κB blockade group. (E) The co-localized expression of TRPM8 and NF-κB was assessed by immunofluorescence detected by confocal microscopy. Both TRPM8 and NF-κB were localized in the cytoplasm in Sham and CCI rat dorsal root ganglion. NF-κB p65 (shown in red) and TRPM8 (shown in red) localized in the same cells. Cellular nuclei were stained with DAPI (shown in blue).