高糖“代谢记忆”介导对血管内皮细胞功能的损伤  

Effects of metabolic memory mediated by high glucose on functional injury of human umbilical vein endothelial cells

作　　者：黎慧清[1] 宋惠杰[1] 廖云飞[1] 刘振华[1] 邓秀玲[1] 张皎月[1] 陈璐璐[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院内分泌科,武汉430022

出　　处：《中华内分泌代谢杂志》2012年第8期669-672,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：国家自然科学基金资助项目（30771035、30800531）

摘　　要：原代人脐静脉内皮细胞分为：正常对照组、持续高糖组、高糖记忆组、渗透压对照组。各组细胞培养第1、4、7天评估内皮细胞增殖、凋亡水平，测定细胞内ROS、SOD、丙二醛活性，eNOSmRNA和蛋白水平，测定内皮细胞上清液中NO水平。高糖组及高糖记忆组人原代脐静脉内皮细胞增殖受到抑制，甘露醇对照组亦受到抑制，高糖使脐静脉内皮细胞凋亡增加，ROS，丙二醛水平升高，SOD水平下降。脐静脉内皮细胞恢复正糖培养后，上述指标未能恢复至正常对照组水平。与正常对照组相比，高糖组及高糖记忆组eNOS及NO水平呈先升高后下降趋势，而高渗对照组与正常对照组相比无差异。结果提示血管内皮细胞存在高血糖代谢记忆现象；短暂高血糖可导致血管内皮细胞持续氧化应激失衡，血管内皮舒张因子NO水平下降，提示氧化应激可能是高血糖“代谢记忆”效应致血管内皮细胞持续损伤的重要机制之一。Cultured primary human umbilical vein endothelial cells （HUVECs） were divided into 4 groups ： normal control（ NG ）, persistent high glucose （ HG ）, hyperglycemia group （ TG ）, and mannitol control （ MA ） groups. After 1,4, and 7 days of culture, cells were collected. Cell proliferation, cell apoptosis, ROS, SOD, MDA, and NO level, eNOS mRNA and protein level were measured. Endothelial cell proliferation was inhibited in HG, TG, and MA groups compared with NG group. Hyperglycemia memory induced apoptosis of endothelial cells, increased ROS and MDA generation, and down-regulated intracellular SOD level, findings similar to those in HG group. After 24 h of culturing, eNOS expression and NO generation in both HG and TG groups were higher than those in NG group. However, ＇after 7 days of culturing, eNOS expression and NO generation in both HG and TG groups were lower than those in NG group. These results suggest that in hyperglycemia memory cell model, transient hyperglysemia may lead to persistent imbalance in oxidative stress and reduee endothelium-derived relaxing factor NO level, indicating that hyperglycemia memory may play an important role in persistent vascular endothelial cell injury.

关 键 词：糖尿病 代谢记忆 氧化应激 一氧化氮 内皮型一氧化氮合酶 

分 类 号：R587.2[医药卫生—内分泌]