医学
再灌注损伤
肾
急性肾损伤
缺血
一氧化氮合酶
肾损伤
缺血预处理
促炎细胞因子
内分泌学
内科学
麻醉
一氧化氮
炎症
作者
Suh Min Kim,Si Wha Kim,Yoo Jin Jung,Sang Il Min,Seung-Kee Min,Sang Joon Kim,Jong‐Won Ha
出处
期刊:Surgery
[Elsevier]
日期:2014-03-01
卷期号:155 (3): 554-561
被引量:14
标识
DOI:10.1016/j.surg.2013.10.005
摘要
3,5,3-triiodothyronine (T3) was found to decrease ischemia-reperfusion (I/R) injury of liver and myocardium in animal models when preconditioned 48 hours in advance of the I/R injury. The purpose of this study was to evaluate the effects of T3 preconditioning on renal I/R injury with different time intervals and to determine the changes in antioxidants, apoptosis, and nitric oxide synthase (NOS) in each condition.In male C57BL/6 mice, renal I/R injury was induced by temporary ligation of the bilateral renal pedicles for 45 minutes followed by a reperfusion period for 24 hours. Preconditioning with intraperitoneal injection of T3 was performed 24 or 6 hours before or at the time of I/R injury.From the histologic examination, tubular injury was decreased in mice preconditioned with T3 6 hours before I/R injury. The levels of proinflammatory cytokines were decreased with T3 preconditioning, either 6 hours or at the time of I/R injury. The levels of glutathione were increased in all treatment groups. Expressions of neuronal NOS were increased when preconditioned 6 hours before or at the time of I/R injury. The number of apoptotic tubular epithelial cell evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay was decreased when preconditioned immediately before I/R injury.Preconditioning with T3 6 hours or immediately before I/R injury had a protective effect on renal I/R injury. The changes of NOS and antiapoptosis, other than well-known antioxidative properties, may play a role in the effect of short-term preconditioning.
科研通智能强力驱动
Strongly Powered by AbleSci AI