关键词:

分裂蛋白 1 , 线粒体分裂 , 凋亡 , 肾缺血 / 再灌注损伤 ,

Abstract:

Objective To investigate the role of fission protein 1 （FIS1） in affecting renal ischemiareperfusion injury by regulating mitochondrial division and apoptosis. Methods Probing FIS1 expression levels and apoptosis levels were measured at different times in the renal tubular epithelial cell（ HK-2）with hypoxiareoxygenation（ HR）model and mouse renal ischemia-reperfusion（ IR） model. Cell lines with FIS1 knockdown and overexpression were constructed，changes in the degree of mitochondrial division were observed using mitochondrial probes，and changes in the level of apoptosis were detected with flow cytometry. Results FIS1 knockdown/ overexpression had essentially no effect in normal cells. After HR， knockdown of FIS1 inhibited mitochondrial division and reduced apoptosis levels， and vice versa after overexpression of FIS1. Conclusion In IRI， Inhibition of FIS1 expression reduces mitochondrial division and reduces the level of apoptosis， which is expected to be a potential therapeutic target for IRI. 

Key words:

Fission protein 1, Mitochondrial division, Apoptosis, Renal ischemia-reperfusion injury