新医学Issue(3)：144-148,5.DOI:10.3969/g.issn.0253-9802.2015.03.003
线粒体功能障碍在晚期糖基化终产物致肾小球内皮细胞通透性增加中的作用机制
Role of mitochondrial dysfunction in advanced glycation end products-induced permeability increases in glomerular endothelial cells
摘要
Abstract
Objective To investigate the effect of advanced glycation end products (AGEs)on the permeability of glomerular endothelial cells (rGEnC)in rats and the role of mitochondrial dysfunction in this pathological process.Methods Primary cultured rGEnC were incubated with AGEs (80 mg/L)for 24 h.The changes in endothelial permeability were investigated by transendothelial electrical resistance and the flux of flu-orescein isothiocyanate-conjugated bovine serum albumin.MitoSOX kit was used to detect intracellular reactive oxygen species (ROS).Mitochondrial membrane potential (△Ψm)was measured by JC1 fluorescein staining.The generation of adenosine triphosphate (ATP)was evaluated by luciferase assay system.The expression of NF-E2-related factor 2 (Nrf2)was detected by western blotting.Results The monolayer permeability and the generation of ROS of rGEnC were increased by AGEs.Pretreatment with tert-Butyl-hydroquinone (tBHQ)(20μmol/L),N-acetylcysteine (NAC)(1 0 mmol/L)and anti-RAGE antibody (1 00 mg/L)could suppress the detrimental effect of AGEs.The decline of △Ψm,ATP and Nrf2 were induced by AGEs,whereas the decrea-ses of △Ψm and ATP could be blocked by pretreatment with anti-RAGE antibody and the decline of △Ψm and Nrf2 inhibited by tBHQ pretreatment.Conclusions AGEs can cause mitochondrial dysfunction,leading to el-evated levels of ROS,which contributes to increase of permeability in rGEnC.关键词
晚期糖基化终产物/线粒体/肾小球内皮细胞/氧化应激Key words
Advanced glycation end products/Mitochondria/Glomerular endothelial cells/Oxidative stress引用本文复制引用
唐骅,李灿明,赖渭妍,饶嘉玲,叶增纯,娄探奇..线粒体功能障碍在晚期糖基化终产物致肾小球内皮细胞通透性增加中的作用机制[J].新医学,2015,(3):144-148,5.基金项目
广东省医学科研基金 （）
