Abstract
(1) Background: Diabetic nephropathy, a microvascular complication of diabetes, is one of the principal causes of end-stage renal disease worldwide. The aim of this study was to explore the therapeutic effects of ergosterol on diabetic nephropathy. (2) Methods: Streptozotocin (STZ)-induced C57BL/6 diabetic mice were treated with ergosterol (10, 20, 40 mg/kg/day) for 8 weeks by oral gavage. The in vitro study employed rat mesangial cells exposed to 30 mM glucose for 48 h in the presence of 10 or 20 μM ergosterol. (3) Results: Ergosterol treatment improved body weights, ameliorated the majority of biochemical and renal functional parameters and histopathological changes, and reduced extracellular matrix (ECM) deposition in diabetic mice. In vitro, ergosterol suppressed proliferation, reduced the levels of ECM proteins, and increased the expression of matrix metalloproteinase-2 and -9 in high glucose-induced mesangial cells; Furthermore, ergosterol markedly improved transforming growth factor-β1 (TGF-β1) expression, enhanced phosphorylation levels of drosophila mothers against decapentaplegic 2 (Smad2), and regulated the downstream factors in vivo and in vitro. (4) Conclusions: Ergosterol alleviated mesangial cell proliferation and the subsequent ECM deposition by regulating the TGF-β1/Smad2 signaling pathway.
Highlights
IntroductionOne of the most serious long-term complications of Diabetes mellitus (DM), has been considered the leading cause of end-stage renal disease (ESRD) [2]
Diabetes mellitus (DM) is a chronic condition that occurs when there are raised blood glucose levels, arises from pancreas’ failure to secret enough insulin and/or decreased response to insulin [1].Diabetic nephropathy, one of the most serious long-term complications of DM, has been considered the leading cause of end-stage renal disease (ESRD) [2]
diabetic nephropathy (DN) is characterized by marked mesangial matrix expansion resulting from from hyperglycemia-induced stress and renal interstitial fibrosis resulting from extracellular matrix (ECM) deposition, hyperglycemia-induced stress and renal interstitial fibrosis resulting from ECM deposition, which which lead to irreversible damage to kidney function [24,25]
Summary
One of the most serious long-term complications of DM, has been considered the leading cause of end-stage renal disease (ESRD) [2]. It is characterized by proteinuria, an expanded mesangial area, a thickening of basement membrane, persistent renal fibrosis, and progressive renal function decline, which are caused by the accumulation of extracellular matrix (ECM) deposition [3]. Glomerular mesangial cells maintain the structural architecture of the glomerular capillary and mesangial matrix homeostasis as well as regulating the filtration surface area [5] These cells can be stimulated by high ambient glucose and undergo over-proliferation, hypertrophy, and increasing
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