Reactive oxygen species contribute to simulated ischemia/reperfusion-induced autophagic cell death in human umbilical vein endothelial cells.

摘要: Background Autophagy is important for cells to degrade protein aggregates and organelles. Our preliminary study suggests that ischemia/reperfusion in rabbit hearts promoted autophagic myocardial injury, resulting no-reflow phenomenon. In this study, we sought further understand the mechanism outcome of upregulation autophagy ischemia/reperfusion. Material methods We employed a simulated (sI/R) model human umbilical vein endothelial (HUVECs) vitro, presence or absence antioxidants. Results confirms sI/R induces HUVECs as measured by increased expression Beclin 1 microtubule-associated light chain 3 (LC3), electron microscopic analysis, special biofluorescent staining with monodansylcadaverine. This sI/R-induced was also accompanied levels p65 cell death. addition, detected accumulation reactive oxygen species (ROS) after sI/R. Moreover, application ROS scavengers block release ROS, were able demonstrate inhibition increases survival. Conclusions The involved death HUVECs.