急性肾损伤
药理学
肾
标记法
细胞凋亡
再灌注损伤
医学
缺血
肾功能
线粒体
内科学
化学
生物化学
作者
Mei Zhang,Rong Dong,Jing Yuan,Jingjing Da,Yan Zha,Yun Long
标识
DOI:10.1111/1440-1681.13601
摘要
Ischaemia-reperfusion (I/R) is one of the main factors of acute kidney injury (AKI). mitochondrial damage pathway are important features of I/R induced-acute kidney injury (IRI-AKI). Hypoxia-inducible factor (HIF) expression in renal tubule segments is up-regulated during AKI. Herein, we investigated the role of FG-4592 in a mouse model of IRI-AKI to confirm whether FG-4592 is beneficial in AKI. We found that pretreatment with FG-4592 significantly ameliorated renal function and renal histological damage in mice after IRI. Furthermore, these results suggest that pretreatment with FG-4592 significantly reduced the tubular cells apoptosis (decreased TUNEL-positive cells, Bax, caspase12 levels), attenuated mitochondrial damage (increased ATPβ, PPARγ, mitochondrial DNA copy number, and decreased cytoplasmic cytochrome C), and alleviated DNA damage after IRI. In conclusion, pretreatment with FG-4592 may effectively prevent kidney from IRI possibly by via diminishing tubular cells injuries and protection of mitochondrial damage pathway. These results further validate that FG-4592 may be an effective drug in the clinical treatment of IRI-AKI.
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