Potential mechanisms underlying the renoprotective effect of empagliflozin, a novel selective sodium glucose co-transporter (SGLT) 2 inhibitor, against diabetic nephropathy in streptozotocin induced diabetic rats

Abstract

Diabetic nephropathy is a major microvascular complication of diabetes and a primary cause of end-stage renal disease worldwide. This study was designed to assess whether control of hyperglycemia with empagliflozin, a new sodium glucose co-transporter (SGLT) 2 inhibitor could improve the renal functions in streptozotocin induced diabetic rats. Thirty two adult male albino rats were randomly assigned into four equal groups. Group I; non diabetic control, Group II; non diabetic rats treated with empagliflozin, group III; diabetic rats and group IV; diabetic rats treated with empagliflozin. Diabetic rats treated with empagliflozin showed significant increase in body weight and significant reduction in Kidney weight, blood glucose and glycated haemoglobin (HbA1c) levels. Empagliflozin also produced significant decrease in blood urea nitrogen (BUN), serum creatinine, urinary albumin excretion (UAE), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and transforming growth factor beta-1 (TGF-β1). It also attenuated Kidney tissue oxidative stress. Empagliflozin showed a renoprotective effect in streptozotocin induced diabetic rats through its glucose lowering effect and by reducing oxidative stress, inflammation, fibrosis and histopathological alterations. SGLT-2 inhibitor seems to be a promising therapeutic strategy for managing diabetes mellitus to slow the progression of diabetic nephropathy.