effectiveness of nicotinamide phosphoribosyltransferase/pre-b cell colony-enhancing factor/ visfatin in preventing high glucose-induced neurotoxicity in an in-vitro model of diabetic neuropathy

Introduction: diabetic neuropathy is a well-known complication of diabetes. recently, hyperglycemia-induced toxicity has been confirmed to participates in multiple cellular pathways typical for neural deterioration. nicotinamide phosphoribosyltransferase/pre-b cell colony-enhancing factor (nampt/pbef)/visfatin is a novel endogenous ligand that some studies have shown its neuroprotective effects on neurodegenerative disease. therefore, we hypothesized that visfatin may prevent high glucose (hg)-induced neurotoxicity by inhibiting apoptosis, autophagy, and reactive oxygen species (ros) responses properly. methods: in this study, pheochromocytoma cell line 12 (pc12) cells were exposed to both hg concentrations (50, 75, 100, 125, 150 mm) and visfatin (50, 100, 150 ng/ml) at different time -points to determine the optimum time and dose of glucose and visfatin. to investigate the effects of visfatin on hg-induced damage in the pc12 diabetic neuropathy model, we examined ros response, apoptosis, and autophagy using ros detection kit, flow cytometry, and real-time pcr/western blot, respectively. results: we determined that hg concentration significantly increased the ros level and apoptosis of diabetic pc12 cells. however, visfatin treatment significantly decreased the ros production (p<0.05) and apoptosis of diabetic pc12 cells (p<0.0001). beclin-1 messenger ribonucleic acid (mrna) level (p<0.05) and light chain 3 (lc3)-ii protein level (p<0.05) showed that the autophagy pathway is impaired by hg concentrations. conclusion: we concluded that visfatin can sufficiently decrease neural damage caused by ros production and apoptosis under hg-induced toxicity.