Abstract
BackgroundDiabetic nephropathy (DN) is one of the major causes of end-stage renal disease in diabetic patients. Increasing evidence from studies in the rodents has suggested that this disease is associated with increased oxidative stress due to hyperglycemia. In the present study, we evaluated the renoprotective, anti-oxidative and anti-apoptotic effects of the flavonoid quercetin in C57BL/6J model of DN.MethodsDN was induced by streptozotocin (STZ, 100 mg/kg/day, for 3 days) in adult C57BL/6J mice. Six weeks later, mice were divided into the following groups: diabetic mice treated with quercetin (DQ, 10 mg/kg/day, 4 weeks), diabetic mice treated with vehicle (DV) or non-treated non-diabetic (ND) mice.ResultsQuercetin treatment caused a reduction in polyuria (~45%) and glycemia (~35%), abolished the hypertriglyceridemia and had significant effects on renal function including, decreased proteinuria and high plasma levels of uric acid, urea and creatinine, which were accompanied by beneficial effects on the structural changes of the kidney including glomerulosclerosis. Flow cytometry showed a decrease in oxidative stress and apoptosis in DN mice.ConclusionTaken together, these data show that quercetin effectively attenuated STZ-induced cytotoxicity in renal tissue. This study provides convincing experimental evidence and perspectives on the renoprotective effects of quercetin in diabetic mice and outlines a novel therapeutic strategy for this flavonoid in the treatment of DN.
Highlights
Diabetic nephropathy (DN) is one of the most important microvascular complications of diabetes mellitus [1,2,3] and is the largest single cause of end stage renal disease [4,5], that leads to a decrease in quality of life and an increased risk of mortality [6]
Diabetic mice exhibited a severe polyuria (24 ± 2 mL/24 h, Figure 1D) when compared to non-diabetic mice (1.9 ± 0.2 mL/24 h), and this parameter was reduced by approximately 46% in diabetic mice treated with quercetin
Body weight was similar among the 3 groups; over the 2-week period, body weight gain in the nondiabetic group (28% g, p < 0.05) neither the diabetic mice nor the diabetic mice treated with quercetin exhibited significant body weight gain (+0.6 ± 1.2 and +1.2 ± 1.0 g, respectively, Figure 1C)
Summary
Diabetic nephropathy (DN) is one of the most important microvascular complications of diabetes mellitus [1,2,3] and is the largest single cause of end stage renal disease [4,5], that leads to a decrease in quality of life and an increased risk of mortality [6]. The development of experimental models of DN has provided a valid approach to characterize its pathogenesis and to create new possibilities for the diagnosis and treatment of this disease. In this regard, the pancreatic islet cell toxin streptozotocin (STZ) has been widely used to induce diabetes in rodents [1,15,16], mainly in rat models. Cumulative evidence suggests that increased oxidative stress may play a crucial role in the pathogenesis of DN [21,22], antioxidant therapy has shown conflicting results during the treatment of DN in diabetic patients [23]. We evaluated the renoprotective, anti-oxidative and anti-apoptotic effects of the flavonoid quercetin in C57BL/6J model of DN
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