Abstract
Diabetic nephropathy (DN) is a diabetic complication marked by albuminuria and a decline of the glomerular filtration rate. Diabetic kidneys are defective in the autophagy process and mitochondrial function and their enhancement of activity alleviates the pathology. In this paper, we developed a mouse model of DN by a combined treatment of a high-fat diet and streptozotocin after unilateral nephrectomy and supplementation with flower or leaf extracts of Abelmoschus manihot (AM) were tested. The preventive effects of the extracts on DN pathology and changes on autophagy and mitochondrial proteins were investigated. DN mice showed a significant increase in fasting blood glucose, plasma creatinine, blood urea nitrogen, and urinary albumin levels. Periodic acid–Schiff and Sirius red staining of the diabetic kidney presented a significant change in glomerular and tubular structures that was associated with podocyte loss and fibrotic protein accumulation. These changes were attenuated by AM extract treatment in DN mice. In addition, hepatic injury, proinflammatory cytokines, and lipid accumulation were decreased by AM extracts in DN mice. As a protective mechanism, AM extracts significantly increased the expression of proteins by regulating autophagy and mitochondrial dynamics, which potentially prevented the kidney and liver from accumulating pathogenic proteins and dysfunctional mitochondria, which alleviated the progression of DN.
Highlights
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease
The mice treated with flower orfunction leaf extracts mice were orally administered with each extract from flowers or leaves for weeks and Huangshukuihua and Dakpul were denoted as HF, HL, DF, and DL
We found a slight decrease in there was no change in weight from the extract treatment (Figure A1A)
Summary
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease. It affects both type I and II diabetics and is clinically marked by proteinuria and a decline of the glomerular filtration rate.Early stage DN exhibits glomerular hypertrophy, mesangial matrix expansion, and basement membrane thickening. Diabetic nephropathy (DN) is a leading cause of end-stage renal disease. It affects both type I and II diabetics and is clinically marked by proteinuria and a decline of the glomerular filtration rate. Stage DN exhibits glomerular hypertrophy, mesangial matrix expansion, and basement membrane thickening. Advanced DN exhibits nodular glomerulosclerosis, mesangiolysis, and tubulointerstitial fibrosis [1]. Control of blood glucose and blood pressure or the renin-angiotensin system (RAS) inhibition can slow, but not prevent, disease progression. DN has become a worldwide health problem. Patients require renal replacement therapy including life-long dialysis or kidney transplantation [2]
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