Abstract
To investigate the effect of polydatin on glucose transporter, blood glucose homeostasis and renal injury in streptozotocin (STZ)-induced diabetic rats. The in vitro inhibitory effect of polydatin on sodium-glucose cotransporter-1 (SGLT1) and 2 (SGLT2) was determined using HEK293 cells. The inhibitory effect of polydatin on GLUT1 and GLUT4 was evaluated using 3T3-L1 adipocytes. Streptozotocin-induced diabetic rats were used for this study. Fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), urea nitrogen, serum creatinine and urinary protein were determined using biochemical analyzer. Histopathological examination was performed on renal tissue. Serum levels of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein 1 (MCP-1) and C-reactive protein (CRP) were also determined. Polydatin significantly inhibited SGLT1/2 and exhibited high selectivity for both GLUT1 and GLUT4. It significantly and dose-dependently decreased hyperglycemia, enhanced urine glucose excretion in the diabetic rats. The polydatin treatment significantly ameliorated symptoms of DN such as polyuria, polydipsia and hyperphagia. The hypoglycemic effect of polydatin was maintained throughout the treatment period. In addition,the levels of IL-1β, TNF-α, MCP-1 and CRP were significantly reduced in treated group. Treatment with polydatin significantly ameliorated most of the structural and morphological changes induced by STZ. Moreover, the levels of urinary protein, serum creatinine and urea nitrogen were significantly reduced after treatment with polydatin. As a potential dual inhibitor of SGLT1/2, polydatin has high selectivity for GLUT1 and GLUT4. Its long-term administration delays the development of DN, protects renal function and ameliorates renal tissue injury.
Highlights
Diabetic nephropathy (DN) is one of the microvascular complications of diabetes mellitus (DM), in which a patient's renal function deteriorates progressively until it develops into end-stage renal disease
Diabetic nephropathy is the result of multi-factor interactions and it is characterized by increased glomerular filtration, thickening of basement membrane and cumulative damage to extracellular matrix [12, 13]
A glycoside extracted from the rhizome of Polygonum cuspidatum L. has a wide range of pharmacological activities, and it is a structural analog of the SGLTs inhibitor, phlorizin
Summary
Diabetic nephropathy (DN) is one of the microvascular complications of diabetes mellitus (DM), in which a patient's renal function deteriorates progressively until it develops into end-stage renal disease. According to World Health Organization (WHO), there are approximately 420 million diabetic patients worldwide, and the incidence of DN is 20 to 30 % [1]. Hyperglycemia alters renal hemodynamics, and over-activates growth factors and cytokines. Increased concentration of urinary protein and decreased concentration of plasma albumin due to glomerular injury results in whole body edema in patients with DN [2]. Maintenance of blood glucose concentration and blood pressure, and diet control are the major strategies for treating DN. Some patients still progress to end-stage renal disease even when they control their blood glucose and blood pressure. The pathogenesis of DN has attracted much attention in recent times
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