Skip to main content
. Author manuscript; available in PMC: 2024 Oct 1.
Published in final edited form as: Brain Behav Immun. 2023 Aug 7;113:401–414. doi: 10.1016/j.bbi.2023.08.005

Fig. 5. Recombinant TIMP3 protein reverses and prevents mechanical and cold allodynia in a mouse model of chemotherapy-induced neuropathic pain.

Fig. 5.

(A) Schematic of the experiment showing the timeline of paclitaxel (PAX) or vehicle injections, pharmacological studies, and immunohistochemistry (IHC) analysis. (B) Representative image and (C) quantification of Timp3 protein in mouse DRG tissue 14 days after first injection of PAX or vehicle control (n = 5). (D, E) Paclitaxel-induced mechanical (von Frey) and (F) cold allodynia (dry ice) are significantly, dose-dependently reversed up to 6 h by single intrathecal administration of recombinant TIMP3 protein (rTIMP3, 3–100 ng/site) delivered at day 14 after chemotherapy injection (n = 4–5). (G) Schematic of experiment showing timeline of PAX injections concomitantly with rTIMP3 or PBS, behavioral tests, transcriptional, and histological analysis. (H, I) Repeated administrations of rTIMP3 (100 ng/site, i.t.) prevent paclitaxel-induced mechanical and cold allodynia (n = 5–6). BL = baseline. Data expressed as mean ± SEM, statistically analyzed by two-tailed t-test (C), two-way ANOVA followed by Sidak’s post hoc test (D, F, H, I), and one-way ANOVA followed by Turkey’s post hoc test (E). *P < 0.05, **P < 0.01, ***P < 0.001.