An in vitro model of warm hypoxia–reoxygenation injury in human liver endothelial cells

BackgroundIschemia–reperfusion or hypoxia–reoxygenation (H-R) injury adversely affects hepatic function following transplantation and major resection; the death of human sinusoidal endothelial cells (SECs) by apoptosis may play a central role in this process. Caspase-3 is an important intracellular protease in the intrinsic and extrinsic pathways of apoptosis.Materials and methodsSECs and EAhy926 cells were exposed to warm hypoxia at 37°C, followed by reoxygenation at 37°C. Activity of caspase-3 was quantified using Western blotting and colorimetric kinase assays.ResultsH-R caused a significant increase in caspase-3 activity compared with controls in both cell types.ConclusionsWarm H-R injury causes apoptotic cell death of SECs and immortalized cells, but with differing patterns of caspase activity.