Dept. of Cellular Biology and Anatomy, Medical College of Georgia, Georgia Health Sciences Univ., Augusta, GA 30912, USA.
Am J Physiol Renal Physiol. 2012 Dec 1;303(11):F1487-94. doi: 10.1152/ajprenal.00352.2012. Epub 2012 Sep 19.
Renal ischemia-reperfusion leads to acute kidney injury (AKI), a major kidney disease associated with an increasing prevalence and high mortality rates. A variety of experimental models, both in vitro and in vivo, have been used to study the pathogenic mechanisms of ischemic AKI and to test renoprotective strategies. Among them, the mouse model of renal clamping is popular, mainly due to the availability of transgenic models and the relatively small animal size for drug testing. However, the mouse model is generally less stable, resulting in notable variations in results. Here, we describe a detailed protocol of the mouse model of bilateral renal ischemia-reperfusion. We share the lessons and experiences gained from our laboratory in the past decade. We further discuss the technical issues that account for the variability of this model and offer relevant solutions, which may help other investigators to establish a well-controlled, reliable animal model of ischemic AKI.
肾缺血再灌注导致急性肾损伤（AKI），这是一种主要的肾脏疾病，其患病率不断增加，死亡率也很高。为了研究缺血性 AKI 的发病机制并测试肾脏保护策略，已经使用了各种体外和体内的实验模型。其中，肾夹闭的小鼠模型较为流行，主要是因为其可获得转基因模型，且动物体型相对较小，适合进行药物测试。然而，小鼠模型通常不太稳定，导致结果存在明显差异。在这里，我们描述了一种详细的双侧肾缺血再灌注小鼠模型的方案。我们分享了过去十年中我们实验室获得的经验教训。我们进一步讨论了导致该模型变异性的技术问题，并提供了相关解决方案，这可能有助于其他研究人员建立一个可控性好、可靠的缺血性 AKI 动物模型。
