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氧化锌纳米粒子缓解链脲佐菌素诱导的 1 型糖尿病大鼠的糖尿病肾病。

Alleviation of diabetic nephropathy by zinc oxide nanoparticles in streptozotocin-induced type 1 diabetes in rats.

机构信息

Department of Bioscience, Faculty of Science, Universiti Teknologi Malaysia, Johor Bahru, Johor, Malaysia.

Department of Biological Sciences, Yarmouk University, Irbid, Jordan.

出版信息

IET Nanobiotechnol. 2021 Jul;15(5):473-483. doi: 10.1049/nbt2.12026. Epub 2021 Mar 10.

DOI:10.1049/nbt2.12026
PMID:34694755
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8675811/
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.

摘要

本研究探讨了氧化锌纳米粒子(ZnONPs)对糖尿病肾病的影响,糖尿病肾病是终末期肾病糖尿病患者死亡的主要原因。通过腹腔注射链脲佐菌素诱导成年雄性大鼠糖尿病。将 ZnONPs 每天腹腔内给予糖尿病大鼠 7 周。糖尿病与血糖水平升高、24 小时尿白蛋白排泄率、肾小球基底膜厚度、肾氧化应激标志物以及转化生长因子-β1、纤连蛋白、胶原-IV、肿瘤坏死因子-α和血管内皮生长因子-A 的肾 mRNA 或蛋白表达增加有关。此外,糖尿病组的nephrin 和 podocin 的表达以及基质金属蛋白酶-9 的 mRNA 表达减少。在对照组中未检测到这些变化,并且 ZnONP 治疗显著预防了这些变化。这些结果表明,ZnONPs 通过改善肾功能、抑制肾纤维化、氧化应激、炎症和异常血管生成以及延缓足细胞损伤的发展,改善了糖尿病肾病大鼠模型中的肾脏损伤。这些发现可能有助于设计 ZnONPs 的临床应用,以防止糖尿病肾病的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/8675811/4e8af8df523b/NBT2-15-473-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/8675811/4e8af8df523b/NBT2-15-473-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/8675811/42d0abfe96a3/NBT2-15-473-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/8675811/7a6c9e2c4227/NBT2-15-473-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/8675811/f4593edacf44/NBT2-15-473-g006.jpg
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