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 2

Effect of MSC on mitochondrial morphology and morphometry on sciatic nerve sensory fibers of mice with OXL-induced chronic neuropathy. Transmission electron micrographs of sciatic nerve cross-sections from nonneuropathic mice (control group) and neuropathic mice treated with vehicle (OXL+vehicle) or with MSC (OXL+MSC). Panels show myelinated (a–c) and unmyelinated (d–f) fibers of the sciatic nerve. Analyses were performed 4 weeks after treatments. Electron micrograph of the control group reveals mitochondria with double intact membrane and absence of vacuolated intramitochondrial spaces and organelles with normal proportion area (arrow) in both myelinated (a) and unmyelinated fibers (d). Vehicle-treated neuropathic mice presented atypical mitochondria, characterized by increased organelle size (arrowhead), presence of vacuole greater than 50% of the mitochondrial area (asterisk), and accumulation of electron-dense amorphous material at the mitochondrial pole (cross), in both myelinated (b) and unmyelinated (e) fibers. MSC-treated neuropathic mice presented fewer mitochondrial morphological alterations in sensory fibers relative to vehicle-treated neuropathic mice (c, f). (g, h) show the percentage of atypical mitochondria found in myelinated and unmyelinated fibers, respectively. . Data are expressed as ; mice per group. Statistical significance relative to the control group (); ^#statistical significance relative to the OXL+vehicle group (), as determined by one-way ANOVA followed by Tukey’s multiple comparison test.

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