Research Paper Volume 13, Issue 1 pp 389—410

DOK3 is involved in microglial cell activation in neuropathic pain by interacting with GPR84

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Figure 6. Administration of pregabalin dramatically prevents mechanical allodynia and inflammatory responses induced by over-expression of DOK3. B129 mice were treated with intrathecal injections of plasmid cDNA (5 μg) for 3 days and fed pregabalin (30 mg/kg/day) simultaneously for 2 weeks. (A) Paw-withdrawal mechanical threshold (PWMT) was evaluated on days 0, 3, 7, and 14. N=8-10, data are presented as means ± SEM. *p < 0.05 vs. baseline (day 0) & p < 0.05 vs. PBS plus plasmid cDNA on day 7. (B) Upregulation of DOK3 in lumbar spinal cords of mice after intrathecal injections of plasmid cDNA for 7 days was assessed by immunohistochemical analysis. Quantities were determined by calculating the integral optical density (IOD). N=8-10, #p < 0.01 vs. control (CON); scale bars, 100 μm and 20 μm. (CF) mRNA levels for DOK3 (C), TNF-α (D), IL-1β (E), and IL-6 (F) in mouse lumbar spinal cord were determined by RT-qPCR on day 7. N=8-10; *p < 0.05; #p < 0.01; NS, not significant for comparisons between the 2 groups connected by the horizontal line.