Naringin reversal of some aspects of diabetic nephropathy in rats type 1 streptozotocin induced diabetes.

Abstract

The role of naringin on streptozotocin-induced diabetic nephropathy was investigated. Male Wister rats (200-300 g) were divided into six groups (n=7). Group A was treated with a vehicle (0.2 ml of 0.1M citrate buffer pH4.5) by a single intraperitoneal injection (IP) and 3.0 ml/kg/BW of distilled water and group B was treated naringin (50 mg/kg/BW) daily. Groups C, D, E and F were rendered diabetic by a single IP of STZ (60 mg/kg/BW) in 0.1M citrate buffer (pH4.5). Diabetes was confirmed after 2 days (48 hours). Group C was treated with subcutaneous insulin (4 U/kg/BW) twice a day while groups D and F were treated with naringin (50 mg/kg/BW) and ramipril (20 mg/kg/BW) which is the drug that is currently used to treat diabetic nephropathy orally, daily, respectively. On day 55, 24-hours urine samples were collected and on day 56 rats were sacrificed; blood samples were collected by cardiac puncture and kidney and liver samples were excised and snap-frozen in liquid nitrogen for further analysis. Diabetic groups (C, D, E and F) showed significant (p<0.001) hyperglycemia, weight loss, polydipsia, polyuria, impaired glucose tolerance and low fasting plasma insulin compared to the controls. Treatment with naringin improved weight loss, polydipsia, fasting plasma glucose and fasting plasma insulin. Naringin decreased fasting blood glucose but did not improve glucose intolerance and it significantly (p<0.001) improved fasting plasma insulin compared to diabetic control. Furthermore, non-treated diabetic groups significantly (p<0.001) showed elevated plasma malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activities compared to the controls. Naringin further reduced renal lipid peroxidation and increased SOD activities in diabetic rats. Moreover, naringin reversed electrolytes retention and also increased glomerular filtration rate in diabetic rats. Naringin therefore ameliorates some aspects of diabetic nephropathy (GFR, serum and urine electrolytes) by reversing oxidative stress associated with DN.