摘要
目的探讨糖基化终末产物对大鼠视网膜微血管内皮细胞核因子κB活化的影响及辛伐他汀的保护作用。方法体外培养大鼠视网膜微血管内皮细胞,制备糖基化终末产物—糖基化白蛋白。应用荧光显微镜观察核因子κB的活化。并观察给予辛伐他汀后视网膜微血管内皮细胞M atrigel上管腔形成的变化及单核细胞趋化蛋白1的表达。结果视网膜微血管内皮细胞无糖基化白蛋白刺激时,核因子κB主要表达在细胞浆;糖基化白蛋白刺激后核因子κB主要表达在核内,作用30 min时达高峰。糖基化白蛋白作用下管腔形成明显增多,单核细胞趋化蛋白1的表达明显增加,加入辛伐他汀后管腔形成明显减少,单核细胞趋化蛋白1的表达明显下降。结论糖尿病视网膜病变中糖基化终末产物发挥重要作用,核因子κB的活化是其关键环节;辛伐他汀可以减少糖基化白蛋白诱导的管腔形成及单核细胞趋化蛋白1的表达。
Aim To investigate the effect of advanced glycation end products（AGE） on the activation of nuclear factor-κB（NF-κB） in rat retinal microvascular endothelial cells（RMEC） of diabetic retinopathy and the protection of simvastatin. Methods Culturing RMEC in vitro and preparing advanced glycation end products-AGE-BSA.Cells were incubated with AGE-BSA,then NF-κB activation was detected by fluorescence microscope.Tube formation and the expression of monocyte chemotactic protein-1（MCP-1） in microvascular endothelial cells in the presence of simvastatin were studied. Results NF-κB was mainly in cytoplasm without AGE-BSA.After RMEC stimulated by AGE-BSA,NF-κB translocated into nucleus,and reached to the peak in 30 min.AGE-BSA could induce the expression of MCP-1 and tube formation.But obvious inhibitory effects were obtained after treatment with the use of simvastatin. Conclusions AGE is crucial in diabetic retinopathy in which the activation NF-κB is important.Simvastatin significantly reduced the AGE-BSA-induced MCP-1 expression and tube formation.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2011年第6期489-492,共4页
Chinese Journal of Arteriosclerosis
关键词
糖基化终末产物
微血管内皮细胞
核因子ΚB
辛伐他汀
Advanced Glycation End Products
Microvascular Endothelial Cells
Nuclear Factor-κB
Simvastatin
作者简介
崔丹，硕士研究生，讲师，研究方向为心血管疾病的发病机制，E-mail为cnlzh2006@126．com。
