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氯化铁诱导的小鼠颈动脉损伤:一种氧化还原病理学模型。

Ferric chloride-induced murine carotid arterial injury: A model of redox pathology.

作者信息

Li Wei, McIntyre Thomas M, Silverstein Roy L

机构信息

Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA ; Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case, Western Reserve University, Cleveland, OH, USA.

Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.

出版信息

Redox Biol. 2013 Jan 26;1(1):50-5. doi: 10.1016/j.redox.2012.11.001. eCollection 2013.

Abstract

Ferric chloride (FeCl3) induced vascular injury is a widely used model of occlusive thrombosis that reports platelet activation in the context of an aseptic closed vascular system. This model is based on redox-induced endothelial cell injury, which is simple and sensitive to both anticoagulant and anti-platelets drugs. The time required for platelet aggregation to occlude blood flow gives a quantitative measure of vascular damage that is pathologically relevant to thrombotic disease. We have refined the traditional FeCl3-induced carotid artery model making the data highly reproducible with lower variation. This paper will describe our artifices and report the role of varying the oxidative damage by varying FeCl3 concentrations and exposure. To explore a maximum difference between experimental groups, adjustment of the selected FeCl3 dose and exposure duration may be necessary.

摘要

氯化铁(FeCl3)诱导的血管损伤是一种广泛应用的闭塞性血栓形成模型,该模型报道了在无菌封闭血管系统中血小板的激活情况。此模型基于氧化还原诱导的内皮细胞损伤,操作简单,对抗凝药和抗血小板药均敏感。血小板聚集导致血流阻塞所需的时间可定量衡量与血栓性疾病病理相关的血管损伤程度。我们改进了传统的FeCl3诱导的颈动脉模型,使数据具有更高的可重复性且变异性更低。本文将描述我们的技巧,并报告通过改变FeCl3浓度和暴露时间来改变氧化损伤的作用。为了探索实验组之间的最大差异,可能需要调整所选的FeCl3剂量和暴露持续时间。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5289/4116643/8a87a2ea87ed/fx1.jpg

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