医学
细胞凋亡
血尿素氮
缺血
肾
肌酐
肾缺血
氧化应激
内科学
内分泌学
泌尿科
再灌注损伤
药理学
麻醉
病理
生物化学
生物
作者
Hui Chen,Bianzhi Xing,Lei Wang,Xiaodong Weng,Zhiyuan Chen,Xiuheng Liu
出处
期刊:Renal Failure
[Taylor & Francis]
日期:2014-08-26
卷期号:36 (10): 1575-1580
被引量:12
标识
DOI:10.3109/0886022x.2014.949769
摘要
Background: Ischemic postconditioning (IPoC) is defined as a series of intermittent interruptions of blood flow in the early phase of reperfusion that mechanically alters the hydrodynamics of reperfusion and it attenuates renal damage after ischemia/reperfusion (I/R) injury in vivo. But all of these data had been obtained in adult populations and whether this protection was maintained in aging kidneys was unknown. The objective of this study was to establish whether the efficacy of IPoC is maintained in aging kidneys. Materials and methods: The aged (24-month-old) and young (3-month-old) Wistar rats were used. Rats were subjected to 45 min of renal ischemia, both with and without treatment with IPoC. Serum urea nitrogen and creatinine levels, histological examination and apoptosis were assessed at 24 h. Oxidative stress was evaluated and apoptosis-related molecules were studied by Western blotting. Results: In young rat kidneys, IPoC significantly attenuated the renal dysfunction and cell apoptosis induced by I/R. In contrast, IPoC failed to limit renal dysfunction, possibly a consequence of increased apoptosis in aged rat kidneys. Conclusions: Our data indicated that IPoC was ineffective in aged rat kidneys. These findings may have major implications in that severe apoptosis in aged kidneys might be refractory to anti-apoptotic effect by IPoC.
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