Rosiglitazone Alleviates Mechanical Allodynia of Rats with Bone Cancer Pain through the Activation of PPAR-γ to Inhibit the NF-κB/NLRP3 Inflammatory Axis in Spinal Cord Neurons

Figure 4

Endogenous expression and cellular localization of proliferator-activated receptor-γ (PPAR-γ). (a, b) Western blot results revealed a significant increase in PPAR-γ expression at 14 and 18 days in bone cancer pain (BCP) rats ( vs. the sham group; , one-way ANOVA (a, b)). There was no difference in the expression of PPAR-γ between rats in the sham group and BCP rats at 7days ( vs. sham group; , one-way ANOVA (a, b)). (c) Immunofluorescence results showed that in the dorsal horn of the spinal cord of BCP rats, PPAR-γ (red) was primarily expressed in neurons (green) rather than the astrocytes (green) or microglia (green). Lumbar enlargements were collected on day 18 after the operation or cancer cell inoculation. Sections were counterstained with DAPI (blue) to label cell nuclei. The white arrows indicate colocalization of PPAR-γ with NeuN (neuronal nuclei, neuronal-specific marker), GFAP (glial fibrillary acidic protein, astrocyte-specific marker), and IBA-1- (ionized calcium binding adapter molecule 1, microglial specific marker) immunoreactive cells in the spinal dorsal horn, respectively; . . represents the number of experimental animals in each group. N.S: not statistically significant.

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