Melatonin protects against hyperglycemia-induced Schwann cells apoptosis through MTOR and Wnt signaling pathways

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Diabetic neuropathy is a commonly reported complication of diabetes mellitus. The current treatment regime could not effectively treat diabetic neuropathy, which is a debilitating condition that approximately afflicts 70% of the patients. Diabetic neuropathy affects both autonomic and peripheral nerves, leading to severe pain, disability and might even fatal at times. Hence it is very important to identify an adjuvant therapy that can protect or minimize the damage from diabetic neuropathy for diabetes patients. It has been reported that Schwann cells dysfunction and apoptosis due to prolonged exposure to high glucose are important pathological features of diabetic neuropathy. Melatonin is a neurohormone secreted by pineal gland and has been reported with multiple beneficial actions such as antioxidant and anti-inflammatory. Thus the present study investigates the potential protective effects of melatonin effective against Schwann cells damage under hyperglycemic condition and studies the underlying mechanisms. Our results showed that melatonin treatment significantly reduced hyperglycemia-induced cell death and increased cell survival. Cell death due to oxidative stress was measured by DCFH-DA assay. Result revealed that hyperglycemia induced oxidative stress was attenuated by melatonin. Moreover, melatonin prevented hyperglycemia induced-Schwann cells mitochondrial membrane potential depletion and cell apoptosis was detected by flow cytometry. Immunoblotting showed that under hyperglycemia condition, Wnt and its co-receptor(Lrp), mTOR , raptor and rictor were down-regulated. Melatonin could protect hyperglycemia-induced cell death through upregulated Wnt, Lrp, mTOR, raptor and rictor protein expression. Our conclusion was melatonin protects against hyperglycemia induced Schwann cells apoptosis through MTOR and Wnt signaling pathways.
Original languageEnglish
Number of pages1
Publication statusPublished - 2016

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