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高车前苷预处理通过抑制足细胞乙酰肝素酶表达来预防糖尿病肾病肾小球基底膜损伤。

Hyperoside pre-treatment prevents glomerular basement membrane damage in diabetic nephropathy by inhibiting podocyte heparanase expression.

机构信息

Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, 201508, China.

Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, 200025, China.

出版信息

Sci Rep. 2017 Jul 25;7(1):6413. doi: 10.1038/s41598-017-06844-2.

DOI:10.1038/s41598-017-06844-2
PMID:28743882
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5527129/
Abstract

Glomerular basement membrane (GBM) damage plays a pivotal role in pathogenesis of albuminuria in diabetic nephropathy (DN). Heparan sulfate (HS) degradation induced by podocyte heparanase is the major cause of GBM thickening and abnormal perm-selectivity. In the present study, we aimed to examine the prophylactic effect of hyperoside on proteinuria development and GBM damage in DN mouse model and the cultured mouse podocytes. Pre-treatment with hyperoside (30 mg/kg/d) for four weeks could significantly decrease albuminuria, prevent GBM damage and oxidative stress in diabetes mellitus (DM) mice. Immunofluorescence staining, Real time PCR and Western blot analysis showed that decreased HS contents and increased heparanase expression in DN mice were also significantly improved by hyperoside pre-treatment. Meanwhile, transmission electron microscope imaging showed that hyperoside significantly alleviated GBM thickening in DN mice. In addition, hyperoside pre-treatment inhibited the increased heparanase gene (HPR1) promoter activity and heparanase expression induced by high glucose or reactive oxidative species (ROS) in cultured podocytes. Our data suggested that hyperoside has a prophylactic effect on proteinuria development and GBM damage in DM mice by decreasing podocyte heparanase expression.

摘要

肾小球基底膜 (GBM) 损伤在糖尿病肾病 (DN) 中的白蛋白尿发病机制中起着关键作用。足细胞肝素酶诱导的硫酸乙酰肝素 (HS) 降解是 GBM 增厚和异常的选择性通透性的主要原因。在本研究中，我们旨在研究淫羊藿苷对 DN 小鼠模型和培养的小鼠足细胞中蛋白尿发展和 GBM 损伤的预防作用。淫羊藿苷 (30mg/kg/d) 预处理四周可显著减少白蛋白尿，预防糖尿病小鼠的 GBM 损伤和氧化应激。免疫荧光染色、实时 PCR 和 Western blot 分析表明，DN 小鼠中 HS 含量降低和肝素酶表达增加也被淫羊藿苷预处理显著改善。此外，电镜成像显示淫羊藿苷可显著减轻 DN 小鼠的 GBM 增厚。此外，淫羊藿苷预处理可抑制高糖或活性氧 (ROS) 诱导的培养足细胞中肝素酶基因 (HPR1) 启动子活性和肝素酶表达的增加。我们的数据表明，淫羊藿苷通过降低足细胞肝素酶表达对 DM 小鼠的蛋白尿发展和 GBM 损伤具有预防作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/9f0fe929a2d7/41598_2017_6844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/1ff1e8031361/41598_2017_6844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/dcc5c00210b3/41598_2017_6844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/62d72e2a9588/41598_2017_6844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/dd6316ee000d/41598_2017_6844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/612da1f71df1/41598_2017_6844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/9f0fe929a2d7/41598_2017_6844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/1ff1e8031361/41598_2017_6844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/dcc5c00210b3/41598_2017_6844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/62d72e2a9588/41598_2017_6844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/dd6316ee000d/41598_2017_6844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/612da1f71df1/41598_2017_6844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6829/5527129/9f0fe929a2d7/41598_2017_6844_Fig6_HTML.jpg

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Nat Rev Nephrol. 2017 Apr;13(4):201-212. doi: 10.1038/nrneph.2017.6. Epub 2017 Feb 6.
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ADA Updates Standards of Medical Care for Patients with Diabetes Mellitus.美国糖尿病协会更新糖尿病患者医疗护理标准。
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