Exercise intervention attenuates neuropathic pain in diabetes via mechanisms of mammalian target of rapamycin (mTOR).

This study was to examine the role of exercise intervention in modulating neuropathic pain induced by diabetes. Diabetes was induced by streptozotocin (STZ, i.p.) in rats and mechanical hyperalgesia was observed three weeks after STZ. Mechanical withdrawal thresholds were increased after four to five weeks of exercise in STZ rats. We also examined the role of signal of mammalian target of rapamycin (mTOR) in regulating neuropathic pain. Inhibition of neuropathic pain by exercise in STZ rats was accompanied with decreases of p-mTOR, p-S6K1, and p-4E-BP1 in sensory nerves. Blocking mTOR also elevated mechanical withdrawal thresholds in STZ rats. Furthermore, pro-inflammatory IL-6 was greater in sensory nerves of STZ rats. Inhibition of IL-6 decreased mTOR and increased mechanical withdrawal thresholds in STZ rats. Overall, our data suggest the role played by exercise in improving neuropathic pain after STZ and that IL-6-mTOR signal is a part of mechanisms engaged in the effects of exercise.

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