Your browser doesn't support javascript.
loading
Damage of endothelial cells induced by OX-LDL and its influence in expressions of TLR-4 and EpCAM / 吉林大学学报(医学版)
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-485587
Biblioteca responsável: WPRO
ABSTRACT
Objective To study the damage effect of oxidized low density lipoprotein (OX-LDL)on the endothelial cells and its influence in the expressions of Toll like receptor 4 (TLR-4)and epithelial cell adhesion molecule (EpCAM).Methods The human endothelial cells ECV-304 were cultured in vitro and treated by different concentrations of OX-LDL for 24 h,and the cell vitality was measured by Taipan blue rejection test.The reactive oxygen species (ROS)level,mitochondrial membrane potential (MMP),cell cycle and apoptosis were detected by flow cytometry (FCM).The expression of TLR-4 and EpCAM were also analyzed by FCM.Results Compared with control group,the ROS levels in ECV-304 cells in 25,50,100,and 200 mg·L-1 OX-LDL were increased, but the cell vitalities and MMP were decreased (P < 0.05).Compared with control group,the percentages of S phase cells in 25 and 50 mg·L-1 OX-LDL groups were increased,the G0 G1 phase cells were slightly reduced,and the SubG1 phase cells (apoptotic cells)were increased with the increasing of OX-LDL concentration.Compared with control group,the TLR-4 and EpCAM expression levels in ECV-304 cells in 50 mg·L-1 OX-LDL group at 24 h were significantly increased (P < 0.05 ). Conclusion OX-LDL could increase the ROS level and induce the apoptosis in vascular endothelial cells,while increase the cell vitality and MMP.During the damage process,the expresion levels of TLR-4 and EpCAM are up-regulated.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Jilin University(Medicine Edition) Ano de publicação: 2015 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Jilin University(Medicine Edition) Ano de publicação: 2015 Tipo de documento: Artigo
...