Abstract
Mesangial cell proliferation contributes to the development of glomerulosclerosis in diabetic nephropathy. This study was aimed at determining whether Osteomeles schwerinae (OSSC) extract can ameliorate renal damage in Spontaneously Diabetic Torii (SDT) rats. OSSC extract (100 and 250 mg/kg/day) was administered to the SDT rats through oral gavage for 17 weeks. At the end of the experiment, glucose, HbA1c, and albuminuria were measured. In addition, the levels of mesangial proliferation-related proteins were determined by western blotting and immunohistochemistry. Our results show that albuminuria, accumulation of the extracellular matrix (ECM), and renal expansion were markedly restored by OSSC extract administration. The OSSC treatment also inhibited α-smooth muscle actin and transforming growth factor-β1 protein expression. In addition, OSSC and its bioactive compounds hyperoside and quercitrin inhibited the platelet-derived growth factor-BB (PDGF-BB)/platelet-derived growth factor-B receptor (PDGFR-β) ligand binding in an in vitro assay. Taken together, these results indicate that OSSC inhibits ECM accumulation and mesangial proliferation of the glomeruli in SDT rats through inhibition of the interaction between PDGF-BB and PDGFR-β. OSSC has ameliorating effects on the initiation and progression of diabetes complications and can be used for the treatment of early diabetic renal dysfunction.
Highlights
Diabetic nephropathy is a serious complication in patients with diabetes
Transforming growth factor-beta1 (TGF-ß1) is a multifunctional cytokine that plays an important role in the regulation of cell proliferation and apoptosis, as well as being a key mediator of diabetic nephropathy that is associated with increased levels of extracellular matrix (ECM) proteins, such as α-smooth muscle actin (α-SMA) and collagen, in renal glomeruli [7]
This study demonstrated that Osteomeles schwerinae (OSSC) treatment markedly ameliorated albuminuria, body weight loss, mesangial expansion, and collagen accumulation in the renal glomeruli of diabetic rats
Summary
Diabetic nephropathy is a serious complication in patients with diabetes This disease is characterized by histological alterations in the renal tissue including thickening of the glomerular basement membrane and mesangial matrix expansion, resulting in the development of glomerulosclerosis [1, 2]. As well as accumulation of extracellular matrix (ECM) components including collagen in the glomeruli, is one of the characteristic pathologic features in the early stages of diabetic nephropathy [3]. Transforming growth factor-beta (TGF-ß1) is a multifunctional cytokine that plays an important role in the regulation of cell proliferation and apoptosis, as well as being a key mediator of diabetic nephropathy that is associated with increased levels of ECM proteins, such as α-smooth muscle actin (α-SMA) and collagen, in renal glomeruli [7]. Increasing evidence shows that TGF-ß1 is key pathogenic factor in the development of renal fibrosis in diabetic nephropathy [8]
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