CAJ | 학술논문

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,eNOS mRNA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.
원대인제정맥내피세포분위:정상대조조、지속고당조、고당기억조、삼투압대조조.각조세포배양제1、4、7천평고내피세포증식、조망수평,측정세포내ROS、SOD、병이철활성,eNOS mRNA화단백수평,측정내피세포상청액중NO수평.고당조급고당기억조인원대제정맥내피세포증식수도억제,감로순대조조역수도억제,고당사제정맥내피세포조망증가,ROS,병이철수평승고,SOD수평하강.제정맥내피세포회복정당배양후,상술지표미능회복지정상대조조수평.여정상대조조상비,고당조급고당기억조eNOS급NO수평정선승고후하강추세,이고삼대조조여정상대조조상비무차이.결과제시혈관내피세포존재고혈당대사기억현상；단잠고혈당가도치혈관내피세포지속양화응격실형,혈관내피서장인자NO수평하강,제시양화응격가능시고혈당“대사기억”효응치혈관내피세포지속손상적중요궤제지일.
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 reduce endothelium-derived relaxing factor NO level,indicating that hyperglycemia memory may play an important role in persistent vascular endothelial cell injury.