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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Targeting prokineticin system counteracts hypersensitivity, neuroinflammation, and tissue damage in a mouse model of bortezomib-induced peripheral neuropathy

Fig. 7

Effect of PC1 chronic treatment on neuroimmune activation in the lumbar spinal cord. a mRNA levels of CD68. b the percentage of GFAP positive area in the spinal cord sections of CTR, BTZ 14 days (day 14 corresponding to c.d. 2.4 mg/kg), BTZ 28 days (day 28, corresponding to c.d. 4.8 mg/kg), and BTZ + PC1 mice. Quantitative analysis of GFAP positive signal (b) was computed as integrated optical density for arbitrary areas (6 sections per animal, 5 animals). Immunofluorescence double staining (c) shows the colocalization (yellow) of PK2 (green) with GFAP (astrocytes, red) in the spinal cord of CTR, BTZ 14 days, BTZ 28 days, and PC1 (BTZ + PC1) mice. Cell nuclei were counterstained with DAPI (blue fluorescence), statistical analysis was performed by means of one-way ANOVA analysis of variance followed by Bonferroni’ s post-test. **p < 0.05, ***p < 0.01 vs CTR. dg mRNA levels of TLR4 and of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 respectively while h reports the levels of the anti-inflammatory cytokine IL-10. All the measurements were performed 14 days after the first BTZ administration, before starting the PC1 treatment (CTR and BTZ groups), and at the end of the BTZ/BTZ + PC1 protocol (CTR, BTZ, BTZ + PC1 groups). mRNA levels, determined by real-time qPCR, were expressed in relation to GAPDH and presented as fold increases over the levels of CTR animals (at the same time point). (a, dh) Data represent mean ± SD of 6 mice/group. At day 14, statistical analysis was performed by means of t test while at day 28 by means of one-way ANOVA followed by Bonferroni’s post-test. ***p < 0.001 vs CTR; °°°p < 0.001 vs BTZ day 28

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