Mitochondrial-Derived Peptide MOTS-c Ameliorates Spared Nerve Injury-Induced Neuropathic Pain in Mice by Inhibiting Microglia Activation and Neuronal Oxidative Damage in the Spinal Cord via the AMPK Pathway

What this study reported

Found lower MOTS-c levels in plasma and spinal dorsal horn of mice with spared nerve injury than in control animals, and reported that intrathecally administered MOTS-c produced antinociceptive effects that were blocked by the AMPK inhibitor dorsomorphin but not by naloxone in these mice. Reported increased spinal AMPKalpha1/2 phosphorylation, reduced proinflammatory cytokine production and microglia activation, and reduced neuronal c-Fos expression and oxidative damage in the spinal dorsal horn, with antinociceptive effects retained after minocycline pretreatment.

Limitations

Group sizes not reported in the abstract; single mouse injury model and sex not stated; mechanistic inference rests largely on pharmacological inhibitors; endpoints are behavioural and molecular surrogates in mice rather than clinical outcomes.