The role of apoptosis and autophagy in the insulin-enhancing activity of oxovanadium(IV) bipyridine complex in streptozotocin-induced diabetic mice.

Metal-based therapies (e.g. Vanadium) possess an attractive proposition in medicinal treatment of diabetes mellitus. Defective insulin secretion can result from impaired β-cell function which is mediated by many process including apoptosis and autophagy. In this study. diabetes was induced by administration of streptozotocin then treatment was performed by vanadyl sulfate and [VO(bpy)2 Cl] Cl.H2O complex. Blood glucose level, AST, ALT, BUN, CR, TCHO, TG and total protein were determined in serum. MDA, NO, erythrocyte GSH and SOD were estimated. LC3 and Caspase 3 levels in pancreatic cells were assessed by flow cytometer. Histopathological investigation of pancreatic tissue was performed. Results of Diabetic group showed a significant increase in transaminases activities, TCHO, TG, MDA, NO and Caspase 3 levels and significant decrease in TP, GSH, SOD and LC3 levels. Oral administration of vanadium complex resulted in normoglycemia, significant increase in blood GSH, SOD, TP and LC3 levels, significant decrease in ALT, AST, BUN, TCHO, TG, MDA and NO and Caspase 3 levels. In addition, proliferative effect of complex prevents islet atrophy. From previous results, the insulin-enhancing effect induced by this complex indicated that this new complex can be a valuable candidate as insulin-enhancing and antioxidant compound than inorganic vanadyl sulfate.