The effect of endurance training on dynein motor protein expression in Wistar male rats sciatic nerves with diabetic neuropathy

Most neurodegenerative diseases are associated with the disruption of axonal transport and this might also be related to diabetes-associated disorders affecting the nervous system. Cytoplasmic dynein is a very important motor driving the movement of a wide range of cargoes toward the minus ends of microtubules. The effects of endurance training on dynein motor protein expression in Wistar male rats sciatic nerves with diabetic neuropathy were investigated.
Twenty one male Wistar rats were divided into three groups: diabetic control (DC: n=7), diabetic trained (DT: n=7) and Healthy control (HC: n=7). Two weeks post STZ injection (45 mg/kg, i.p.), rats were subjected to treadmill exercise for 5 days a week for over 6 weeks. Levels of mRNA and protein content were determined by Real time-PCR and ELISA.
The blood glucose levels and dynein mRNA in both sensory and motor parts and dynein content in sciatic nerves were increased by diabetes (P≤0.05). Furthermore, exercise training modulated the dynein mRNA and dynein content to normal levels in diabetic trained rats (P≤0.05). Moreover, exercise training reduced blood glucose levels in the DT rats (P≤0.05).
The results of the present study confirm that dynein expresses up-regulation in STZ-induced diabetic rats. Increase in the amount of dynein expression can be a compensatory response in the lower trophic support and burden imposed on autophagy system. These alterations suggest that retrograde axonal transport may be impaired in diabetic rats. In addition, endurance training as a non-pharmacotherapy strategy can modulate these alterations.