Iranian Journal of

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Background: Diabetic neuropathy is one of the most common complications of diabetes mellitus, which is associated with a decrease in the synthesis and transport of neurotrophins . The aim of present study was to investigate the effect of endurance training on gene expression of nerve growth factor (NGF) in the sensory spinal cord of rats with diabetic neuropathy. Methods: Twenty eight adult male Wistar rats in the body mass range of 326.3±8.4 gr, randomly assigned in to four groups: diabetic control, diabetic training, healthy control and healthy training. For inducing diabetic neuropathy, after twelve hours of food deprivation, intraperitoneal injection of STZ solution (45 mg/Kg) method was used. Two weeks after STZ injection, the endurance training protocol was performed for six weeks and Twenty four hours after the last training session, rats were sacrificed. Gene expression of NGF in rat spinal sensory segments were measured with Real time technique. In order to determine the significant differences between groups and Interaction independent variables two way anova and LSD post hoc test were used. Results: Endurance training, resulted in a significant increase in gene expression of NGF in the rats. Also, in compare with diabetic control, training led to significant decrease in blood glucose levels in diabetic training group. Conclusion: Increased physical activity and exercise can strongly affect pathological factors associated with diabetic neuropathy by increasing nerve growth factor. It is recommended that for prevention of neurological complications and treatment of diseases associated with diabets exercise training could be used as a non-pharmachological treatment.

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Background: Glycogen synthase kinase 3 beta is a key regulator of many signaling pathways. It is reported that Inhibition of this kinase results neuronal survival. Accordingly in this study we investigated the effect of endurance training on the gene expression of GSK-3β in the sensory areas of the spinal cord of male Wistar rats with diabetic neuropathy.

Methods: we randomly assigned 16 male Wistar rats into four groups: healthy control, healthy trained, neuropathy control, neuropathy trained. Intraperitoneal injection of a STZ (streptozotocin) solution (45 mg/kg) was used to induce diabetes. At two weeks after STZ injections, the mechanical allodynia and thermal hyperalgesia tests demonstrated the presence of diabetic neuropathy. A moderate endurance training protocol was performed for a six- week period. At 24 hours after the final training session, the rats were sacrificed and the L4-L6 sensory neurons of the spinal cord tissue were removed. GSK-3β mRNA expression was performed using real time-PCR.

Results: Statistical analysis shows that neuropathy trained experiences a decrease in gene expression in comparison to neuropathy control (P=0.02). On the other there was significant difference between healthy control and neuropathy control (P=0.02). However, there was no significant difference between healthy control and neuropathy trained.

Conclusion: we claim that endurance training will effectively decrease the expression of GSK-3β in the sensory areas of spinal cord of male Wistar rats with diabetic neuropathy. Endurance training as a non- pharmacotherapy strategy can modulate and return GSK-3β to approximate normal levels.