| dc.description.abstract | Diabetes is a common metabolic disease which leads to diabetic peripheral neuropathy.
Recently, the role of microRNA-96 (miR-96) in alleviating neuropathic pain by inhibiting the
expression of NaV1.3, an isoform of voltage-gated sodium channels, has been shown. Peripheral
nerve injuries result in NaV1.3 elevation. Exercise has beneficial role in diabetes management and
peripheral neuropathy. However, the effects of exercise on miR-96 and its target gene NaV1.3 in
diabetic rats are unknown. Therefore, the present study investigated the effects of exercise training
on the expression of miR-96 and NaV1.3 in diabetic rats. For this purpose, rats were randomly
divided into four groups: control, exercise, diabetic and diabetic-exercise groups. Type 2 diabetes
was induced by a high-fat diet and the administration of streptozotocin (STZ) (35 mg/kg, i.p.). The
exercise groups were subjected to swimming exercise 5 days/week for 10 weeks. At the end of the
treatment period, thermal pain threshold, determined through the tail-flick test, and the expression
levels of miR-96 and its target gene NaV1.3 were determined by reverse transcription (RT)-PCR in
the sciatic nerve tissues of the rats. Data of the present study indicated that diabetes diminished
miR-96 expression levels, but significantly upregulated NaV1.3 expression in the sciatic nerve. On
exercise training, miR-96 expression was reversed with concurrent down-regulation of the NaV1.3
expression. This study introduced a new and potential miRNA-dependent mechanism for exerciseinduced
protective effects against diabetic thermal hyperalgesia. | |
