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铁鳌合剂去铁胺通过减轻大鼠炎症和纤维化缓解糖尿病肾病进展。

Iron Chelator Deferoxamine Alleviates Progression of Diabetic Nephropathy by Relieving Inflammation and Fibrosis in Rats.

机构信息

Department of Endocrinology and Metabolism, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

MoE Key Laboratory of Molecular Animal Nutrition, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.

出版信息

Biomolecules. 2023 Aug 18;13(8):1266. doi: 10.3390/biom13081266.

DOI:10.3390/biom13081266
PMID:37627331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10452339/
Abstract

Diabetic nephropathy (DN) is one of the most devastating diabetic microvascular complications. It has previously been observed that iron metabolism levels are abnormal in diabetic patients. However, the mechanism by which iron metabolism levels affect DN is poorly understood. This study was designed to evaluate the role of iron-chelator deferoxamine (DFO) in the improvement of DN. Here, we established a DN rat model induced by diets high in carbohydrates and fat and streptozotocin (STZ) injection. Our data demonstrated that DFO treatment for three weeks greatly attenuated renal dysfunction as evidenced by decreased levels of urinary albumin, blood urea nitrogen, and serum creatinine, which were elevated in DN rats. Histopathological observations showed that DFO treatment improved the renal structures of DN rats and preserved podocyte integrity by preventing the decrease of transcripts of nephrin and podocin. In addition, DFO treatment reduced the overexpression of fibronectin 1, collagen I, IL-1β, NF-κB, and MCP-1 in DN rats, as well as inflammatory cell infiltrates and collagenous fibrosis. Taken together, our findings unveiled that iron chelation via DFO injection had a protective impact on DN by alleviating inflammation and fibrosis, and that it could be a potential therapeutic strategy for DN.

摘要

糖尿病肾病（DN）是糖尿病最严重的微血管并发症之一。先前已经观察到，糖尿病患者的铁代谢水平异常。然而，铁代谢水平如何影响 DN 的机制尚不清楚。本研究旨在评估铁螯合剂去铁胺（DFO）在改善 DN 中的作用。在这里，我们通过高碳水化合物和高脂肪饮食以及链脲佐菌素（STZ）注射建立了 DN 大鼠模型。我们的数据表明，DFO 治疗 3 周可显著改善肾功能障碍，表现为尿白蛋白、血尿素氮和血清肌酐水平降低，而这些指标在 DN 大鼠中升高。组织病理学观察表明，DFO 治疗通过防止足细胞内nephrin 和 podocin 转录物的减少，改善了 DN 大鼠的肾脏结构并维持了足细胞的完整性。此外，DFO 治疗还降低了 DN 大鼠中纤维连接蛋白 1、胶原 I、IL-1β、NF-κB 和 MCP-1 的过度表达，以及炎症细胞浸润和胶原纤维形成。总之，我们的研究结果表明，通过减轻炎症和纤维化，DFO 注射的铁螯合作用对 DN 具有保护作用，它可能是一种治疗 DN 的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9e680497dbb7/biomolecules-13-01266-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/d730e3b85b32/biomolecules-13-01266-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9c51d34fe214/biomolecules-13-01266-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/d4152fa1121b/biomolecules-13-01266-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/45dbc5de5b5f/biomolecules-13-01266-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/4be44f0d4769/biomolecules-13-01266-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9a47ea863b3f/biomolecules-13-01266-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/b84f55f4253e/biomolecules-13-01266-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9e680497dbb7/biomolecules-13-01266-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/d730e3b85b32/biomolecules-13-01266-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9c51d34fe214/biomolecules-13-01266-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/d4152fa1121b/biomolecules-13-01266-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/45dbc5de5b5f/biomolecules-13-01266-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/4be44f0d4769/biomolecules-13-01266-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9a47ea863b3f/biomolecules-13-01266-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/b84f55f4253e/biomolecules-13-01266-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5575/10452339/9e680497dbb7/biomolecules-13-01266-g008.jpg

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