Antioxidant therapy of type 2 diabetic peripheral neuropathy

Abstract

Diabetic peripheral neuropathy (DPN) is a nerve damage caused by chronically high blood glucose and dia-betes. It leads to loss of sensation and sometimes pain in feet, legs and hands. More than 50% of type 2 diabetic patients will develop this complication. To date, the pathogenesis of DPN remains unclear. However, hyperglycemia, metabolic imbal-ance, and oxidative stress appear in the neurons of DPN patients. In addition, oxidative stress results in the change of poly-ADP-ribose polymerase, advanced glycation end products, polyol, protein kinase C, and hexosamine and causes endothelial cell damage and vascular dysfunction, consequently causing peripheral nerve ischemia and hypoxia. According to the oxi-dative stress and related pathways of DPN, some drugs are used in clinical treatment, such as taurine, acetyl-L-carnitine, aldose reductase inhibitors (epalrestat, ranirestat), α-lipoic acid (ALA), protein kinase C inhibitor (ruboxistaurin), inhibitor of poly ADPribose polymerase (nicotinamide), angiotensin-converting enzyme inhibitor (trandolapril), and advanced gly-cation end product inhibitors (aspirin, benfotiamine). However, no drugs can completely cure it. In this review, we sum-marize the pathogenesis of DPN and suggest that amifostine, which is clinically used as an antioxidant, might be used for the treatment of DPN.