Suppr超能文献

1,2,3,4,6-五-O-没食子酰基-β-D-葡萄糖可减弱肾细胞迁移、透明质酸表达及晶体黏附。

1,2,3,4,6-penta-O-galloyl-beta-D-glucose attenuates renal cell migration, hyaluronan expression, and crystal adhesion.

作者信息

Lee Jae-Ho, Yehl Matthew, Ahn Kwang Seok, Kim Sung-Hoon, Lieske John C

机构信息

Department of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.

出版信息

Eur J Pharmacol. 2009 Mar 15;606(1-3):32-7. doi: 10.1016/j.ejphar.2009.01.024. Epub 2009 Jan 25.

Abstract

Calcium oxalate monohydrate (COM) crystals bind avidly to the surface of proliferating and migrating renal endothelial cells, and oxalate-induced peroxidative injury can promote crystal attachment to renal epithelial cells. 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG), isolated from a traditional herbal remedy, inhibits vascular endothelial growth factor (VEGF) stimulated proliferation and migration of human umbilical vein endothelial cells (HUVECs) and has antioxidant activity. This study was performed to determine if PGG altered calcium oxalate monohydrate (COM) crystal adhesion to cells, perhaps via a change in cell surface properties. PGG significantly decreased COM crystal adhesion to cultured MDCK I cells at a low concentration (<10 microM) which was not cytotoxic. PGG exerted anti-adhesion effects whether cells or crystals were pre-coated. PGG also inhibited cell migration after scrape-wounding, decreased subsequent adhesion of crystals to proliferating and migrating cells, and decreased expression of the crystal binding molecule hyaluronan. These findings suggest that PGG represents a potential urolithiasis prevention compound. Anti-crystal adhesion effects appear multifaceted involving crystal coating by PGG, as well as decreased cell migration and the associated surface expression of hyaluronan. The latter represents a novel mechanism of nephrolithiasis prevention.

摘要

一水合草酸钙(COM)晶体可紧密结合于增殖和迁移的肾内皮细胞表面,且草酸盐诱导的过氧化损伤可促进晶体附着于肾上皮细胞。从一种传统草药中分离出的1,2,3,4,6 - 五 - O - 没食子酰基 - β - D - 葡萄糖(PGG)可抑制血管内皮生长因子(VEGF)刺激的人脐静脉内皮细胞(HUVECs)增殖和迁移,并具有抗氧化活性。本研究旨在确定PGG是否通过改变细胞表面特性来改变一水合草酸钙(COM)晶体与细胞的黏附。低浓度(<10 microM)的PGG可显著降低COM晶体与培养的MDCK I细胞的黏附,且该浓度无细胞毒性。无论细胞或晶体预先包被,PGG均具有抗黏附作用。PGG还可抑制刮伤后的细胞迁移,减少晶体随后与增殖和迁移细胞的黏附,并降低晶体结合分子透明质酸的表达。这些发现表明PGG是一种潜在的预防尿石症的化合物。抗晶体黏附作用似乎具有多方面性,涉及PGG对晶体的包被,以及细胞迁移减少和透明质酸相关表面表达降低。后者代表了一种预防肾结石的新机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验