作者: Xiaonan Li , Yuanyuan Rong , Mei Zhang , Xing Li Wang , Scott A. LeMaire
DOI: 10.1016/J.BBRC.2009.02.132
关键词:
摘要: Oxidative stress induced by hyperglycemia is a key factor in the development of cardiovascular diseases diabetes. Thioredoxin (Trx) system, major thiol antioxidant regulates reduction intracellular reactive oxygen species (ROS). In this study, we demonstrated that high glucose significantly increased ROS levels human aortic endothelial cells (HAECs). Additionally, reduced activity thioredoxin. To investigate mechanisms involved, found enhanced expression thioredoxin interacting protein (Txnip), Trx inhibitory protein, through p38 mitogen-activated kinase (MAPK). We also showed regulated Txnip at transcription level and MAPK forkhead box O1 transcriptional (FOXO1) were involved process. Taken together, upregulation subsequent impairment antioxidative system FOXO1 may represent novel mechanism for glucose-induced increase ROS.