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Swimming Exercise Induced Reversed Expression of miR-96 and Its Target Gene NaV1.3 in Diabetic Peripheral Neuropathy in Rats

摘要


Diabetes is a common metabolic disease which leads to diabetic peripheral neuropathy (DPN). Recently, the role of micro-ribonucleic acid-96 (miR-96) in alleviating neuropathic pain by inhibiting the expression of Na_V1.3, an isoform of voltage-gated sodium channels, has been shown. Peripheral nerve injuries result in Na_V1.3 elevation. Exercise has beneficial role in diabetes management and peripheral neuropathy. However, the effects of exercise on miR-96 and its target gene Na_V1.3 in diabetic rats are unknown. Therefore, the present study investigated the effects of exercise training on the expression of miR-96 and Na_V1.3 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 Na_V1.3 were determined by reverse transcription -polymerase chain reaction (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 Na_V1.3 expression in the sciatic nerve. On exercise training, miR-96 expression was reversed with concurrent down-regulation of the Na_V1.3 expression. This study introduced a new and potential miRNA-dependent mechanism for exercise-induced protective effects against diabetic thermal hyperalgesia.

關鍵字

diabetic neuropathy exercise miR-96 Na_V1.3 rat sciatic

參考文獻


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