期刊
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
卷 49, 期 2, 页码 311-318出版社
WILEY
DOI: 10.1111/1440-1681.13601
关键词
acute kidney injury; apoptosis; FG-4592; ischaemia-reperfusion injury; mitochondrial damage
资金
- National Natural Science Foundation of China [81760125]
- Science & Technology Foundation of Guizhou Province [QKHJC[2016]1087]
- Guizhou High-level Innovative Talents Program [QKHPTRC(2018)5636]
The study demonstrates that pretreatment with FG-4592 can effectively improve renal function and histological damage in mice with IRI, potentially by reducing tubular cell injuries and protecting the mitochondrial damage pathway. These results suggest that FG-4592 may be a promising drug for the clinical treatment of IRI-AKI.
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 ATP beta, PPAR gamma, 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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