Abstract
The Psoralea corylifolia L. seed (PCS) is a widely used herbal medicine, but its possible effect against diabetic nephropathy has not been studied. To investigate the anti-nephropathic effect of PCS extracts, we performed experiments using a diabetic mouse model and high glucose-treated mesangial cells. Streptozotocin (STZ)-induced diabetic mice were orally administered PCS extract for 8 weeks (500 mg/kg/day). Increased creatinine clearance, urine volume, urine microalbumin, and mesangial expansion were observed in STZ-induced diabetic mice; these were significantly reduced by PCS extract administration. PCS extract significantly reduced fibrosis in the kidney tissue of diabetic mice as evidenced by decreased mRNA expression of collagen type IV-α2, fibronectin, PAI-1, and TGF-β1. In addition, cleaved PARP, an apoptotic gene, was upregulated in the diabetic nephropathy mice, and this was ameliorated after PCS extract treatment. Treatment of high glucose-treated MES-13 cells with isopsoralen and psoralen, major components of PCS extract, also decreased the expression of fibrosis and apoptosis marker genes and increased cell viability. PCS extract exerts protective effects against STZ-induced diabetic nephropathy via anti-fibrotic and anti-apoptotic effects. PCS extract might be a potential pharmacological agent to protect against high glucose-induced renal damage under diabetic conditions.
Highlights
Diabetic nephropathy is a common microvascular complication in diabetic patients, which leads to high morbidity and mortality throughout the world [1,2]
Body weight was significantly reduced in STZ-induced diabetic mice compared with control weight wastreatment significantly in STZ-induced mice compared with control mice mice and extract didreduced not recover the reduceddiabetic body weight (Figure 1A)
Food food intake and urine volume were increased in STZ-induced diabetic mice compared with control intakeAfter and urine volumeadministration, were increasedwater in STZ-induced diabetic micesignificantly compared with control mice
Summary
Diabetic nephropathy is a common microvascular complication in diabetic patients, which leads to high morbidity and mortality throughout the world [1,2]. Diabetic nephropathy is characterized by structural as well as functional abnormalities. Urinary albumin excretion along with extracellular matrix accumulation, basement membrane thickening, mesangial hypertrophy, and glomerular epithelial cell (podocyte) loss within the glomeruli are characteristic pathological features of diabetic nephropathy [3,4]. Changes in glomeruli such as fibrosis and apoptosis of mesangial cells play important roles in the progression of diabetic nephropathy. The hyperglycemic condition induces expression of genes associated with fibrosis, such as transforming growth factor-β (TGF-β), fibronectin, collagen type IV, α2 (Col4a2), and plasminogen activator inhibitor-1 (PAI-1) [5,6]. Activation of Nutrients 2017, 9, 828; doi:10.3390/nu9080828 www.mdpi.com/journal/nutrients
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