Abstract
This study examines the effect of nanoparticles with zinc oxides (ZnONPs) on diabetic nephropathy, which is the primary cause of mortality for diabetic patients with end‐stage renal disease. Diabetes in adult male rats was induced via intraperitoneal injection of streptozotocin. ZnONPs were intraperitoneally administered to diabetic rats daily for 7 weeks. Diabetes was associated with increases in blood glucose level, 24‐h urinary albumin excretion rate, glomerular basement membrane thickness, renal oxidative stress markers, and renal mRNA or protein expression of transforming growth factor‐β1, fibronectin, collagen‐IV, tumour necrosis factor‐α and vascular endothelial growth factor‐A. Moreover, the expression of nephrin and podocin, and the mRNA expression of matrix metalloproteinase‐9 were decreased in the diabetic group. These changes were not detected in the control group and were significantly prevented by ZnONP treatment. These results provide evidence that ZnONPs ameliorate the renal damage induced in a diabetic rat model of nephropathy through improving renal functionality; inhibiting renal fibrosis, oxidative stress, inflammation and abnormal angiogenesis; and delaying the development of podocyte injury. The present findings may help design the clinical application of ZnONPs for protection against the development of diabetic nephropathy.
Highlights
Diabetic nephropathy (DN) is a significant diabetic microvascular complication
Usual DN histological changes include thickening in both the tubular basement membrane (TBM) and the glomerular basement membrane (GBM), mesangial expansion, and afferent and efferent arteriolar hyaline deposition [3]
Our results showed that matrix metalloproteinase‐9 (MMP‐9) mRNA expression was decreased in the D group compared with the ND group (Figure 5d, P < 0.05), and zinc oxide nanoparticles (ZnONPs) treatment significantly rescued MMP‐9 mRNA levels in the ZnONPs + D group compared with that in the D group (P < 0.05)
Summary
Diabetic nephropathy (DN) is a significant diabetic microvascular complication. The incidence of DN has continued to increase with the expanding cohort of diabetes patients around the world [1] and has become a leading cause of chronic kidney disease in developed countries [2]. It has been established that podocyte apoptosis, necrosis or the loss of their adhesive interaction lead to podocyte detachment from GBM. These cellular pathologies underlie the progression of DN and cause leakage of albumin into the urine [3,4]. Many molecular pathways may affect DN progression These pathways include ECM protein deposition, cellular hypertrophy, oxidative stress, inflammation and apoptosis. Zn deficiency can cause albuminuria enhancement and ECM protein expression through the activation of renal interstitial fibroblasts via the TGF‐β/Smad2/3 pathway, which is correlated with diabetic renal interstitial fibrosis [12]. This study evaluates the possible therapeutic effect of ZnONPs on DN in a streptozotocin (STZ)‐induced rat model of type 1 diabetes
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