کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4301427 | 1288437 | 2012 | 7 صفحه PDF | دانلود رایگان |
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.
Journal: Journal of Surgical Research - Volume 178, Issue 1, November 2012, Pages e35–e41