Effect Of Cellgevity®, A Glutathione-Enhancer Dietary Supplement, On Streptozotocin-Induced Type-2 Diabetes And Nephrotoxicity In Rat

ABSTRACT Background: Diabetic nephropathy (DN), a diabetes-induced nerve damaging effect on the kidney structure and function due to hyperglycaemia is a major microvascular complication. Hyperglycaemia causes uremia, hypercreatininemia, declined glomerular filtration rate, and decreased levels of serum protein and albumin. This condition leads to progressive decline in renal function resulting in renal insufficiency and End-Stage Renal Disease. The prevalence of DN in Africa has increased significantly in recent years, emphasising the importance of developing new preventive and treatment therapies. Despite the fact that there are different medications used to manage DN, most of these drugs are associated with serious unwanted side effects that contributes to the many complications observed in DN patients. This has paved way for the search for newer and better therapeutic agents that can better manage the disease and, at the same time, causing very less side effects. It was hypothesised that Cellgevity® could provide protection from diabetes and its complications. Aim: To evaluate the hypoglycaemic and nephroprotective potentials of Cellgevity® in healthy and type-2 diabetic nephropathy rat models. Methods: Seventy (70) male Sprague-Dawley rats with an average weight of 200 g were grouped into10 groups of seven rats each (n = 7). All rats were subjected to an overnight fast for 12 hours after which type-2 diabetes mellitus (T2DM) was induced using streptozotocin (STZ) (60 mg/kg b.wt) and nicotinamide (NA) (110 mg/kg b.wt). After 24-hours of STZ-NA injection, rats with fasting blood glucose (FBG) greater than 11.1 mmol/L were considered diabetic and divided into 8 groups. Group 1 of the diabetic rats received distilled water (diabetic negative control). Groups 2, 3, and 4 were orally administered with varying doses of Cellgevity® (40 mg/kg b.wt; 80 mg/kg b.wt; 160 mg/kg b.wt respectively); Group 5 and 6 received 15 mg/kg b.wt and 20 mg/kg b.wt of glibenclamide (Glib) and captopril (Cap) respectively. Group 7 and 8 of the diabetic rats received combinations of either Cellgevity® and Glib or Glib and Cap. Two additional groups (non-diabetic rats) served as normal controls. Blood samples were taken by tail snip and FBG were measured at specific days (1, 3, 6, 9, 12, 15, 22 and 29) following induction of T2DM. At the end of the experiment (29th day), the animals were sacrificed, and their blood, kidneys and pancreas harvested for haematological, biochemical, and histological studies. Results: Diabetic rats showed a significant increase in FBG (30.33 mmol/L, p