科研之友
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摘要
Aim: In the course of ischemia reperfusion, injury / functional deterioration of the endothelium contribute to tissue damaging process. Hypoxia-reoxygenation model has been used as in vitro model of ischemia reperfusion injury. Oxygen glucose deprivation model can be considered to mimic the in vivo conditions. This study aimed to develop an in vitro model of ischemia reperfusion injury in human brain micro vascular endothelial cells and to evaluate the cell injury caused.
Methods: Oxygen glucose deprivation injury was produced by the deprivation of glucose during the hypoxia exposure. Cell injury was assessed by lactate dehydrogenase activity, while production of reactive oxygen species was determined using a fluoro-metric assay.
Results: Reoxygenation plus glucose supplementation for 18 and 24 hours, after 6 hours of oxygen glucose deprivation, was observed to cause a significant lactate dehydrogenase release and cell injury. In addition, after 6 hours of oxygen glucose deprivation, reactive oxygen species were found to be maximally increased in the 60(th) minute of reoxygenation plus glucose supplementation.
In conclusion, by oxygen glucose deprivation + reoxygenation + glucose supplementation, a significant lactate dehydrogenase release and an increase in reactive oxygen species was determined and in vitro model of ischemia reperfusion injury in human brain microvascular endothelial cells was achieved. Thus, this model and the different durations of hypoxia-reoxygenation can be used in future studies to investigate the effects of protective agents.
- 出版日期2010
