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

摘要：

目的 探讨分裂蛋白 1（fission protein 1，FIS1）通过调节线粒体分裂及凋亡影响肾缺 血 /再灌注损伤的作用。 方法 分别在肾小管上皮细胞（HK-2）缺氧 / 复氧（hypoxia-reoxygenation， HR）模型和小鼠肾缺血 / 再灌注（ischemia-reperfusion，IR）模型中探究不同时间 FIS1 表达水平及凋亡水平。 构建 FIS1 敲减和过表达的稳转株，用线粒体探针观察线粒体分裂程度的变化，流式细胞仪检测凋亡水平的 变化。 结果 FIS1 敲减 / 过表达在正常细胞中基本没有影响， HR 后，敲减 FIS1 抑制了线粒体分裂，细胞 凋亡水平降低，过表达 FIS1 后结果相反。 结论 IRI 中，抑制 FIS1 的表达能够减少线粒体分裂，降低凋 亡水平，有望成为 IRI 的潜在治疗靶点。 

关键词:

分裂蛋白 1 , 线粒体分裂 , 凋亡 , 肾缺血 / 再灌注损伤 ,