Reestablishment of Redox Homeostasis in the Nociceptive Primary Afferent as a Mechanism of Antinociception Promoted by Mesenchymal Stem/Stromal Cells in Oxaliplatin-Induced Chronic Peripheral Neuropathy

Figure 1

Pain-like behaviors of mice treated with MSC or gabapentin on the OXL-induced painful neuropathy model. (a, b) show mechanical nociceptive threshold data: the strength of the filament (grams) in which the animal responds in 50% of the presentations (-axis) in relation to time (-axis), given in weeks (a) or days (b), after induction of the neuropathy model. (c, d) show cold thermal hyperalgesia data: the frequency of nociceptive behaviors (-axis) in relation to time (-axis), given in weeks (c) and days (d), after OXL induction. The nociceptive threshold was evaluated in the mice before (b) and after OXL induction (week 0). The control group represents nonneuropathic mice that received vehicle (5% dextrose) instead of OXL. Two weeks after the model induction, mice were intravenously treated with MSC (OXL+MSC; ) or vehicle (OXL+vehicle; 100 μL) or orally treated with gabapentin (OXL+GBP; 70 mg/kg; 12/12 h; 6 consecutive days) or saline (OXL+saline; 12/12 h; 6 consecutive days). During the 6 days of GBP treatment, nociceptive thresholds were daily assessed in two moments: immediately before and one hour after the GBP administration. (b, d) show nociceptive threshold data before (time points 1, 2, 3, 4, 5, and 6) and after (time points , , , , , and ) the administration of GBP. Data are expressed as ; mice per group. Statistical significance relative to the control group (); ^#statistical significance relative to the OXL+vehicle group (); ⁺statistical significance relative to the OXL+saline group (), as determined by two-way ANOVA followed by Bonferroni posttest.

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