分裂蛋白1在肾缺血/再灌注损伤中的作用研究  

Studies on the role of fission protein 1 in renal ischemia-reperfusion injury

作　　者：汪海龙 王华彬 徐畅宏 张亚龙 李轶[1] 满江位 程堃 董雅嘉 杨立[1] Wang Hailong;Wang Huabin;Xu Changhong;Zhang Yalong;Li Yi;Man Jiangwei;Cheng Kun;Dong Yajia;Yang Li(Department of Urology,The Second Hospital of Lanzhou University,Gansu Lanzhou 730030,China.)

机构地区：[1]兰州大学第二医院泌尿外科,甘肃兰州730030

出　　处：《实用器官移植电子杂志》2025年第2期136-140,共5页Practical Journal of Organ Transplantation(Electronic Version)

基　　金：中央引导地方科技发展专项(24ZYQA050);省青年科技基金计划(22JR5RA1018);萃英科技创新计划(CY2023-MS-B09);兰州市科技局科技计划(2023-4-39)。

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。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.

关 键 词：分裂蛋白1 线粒体分裂 凋亡 肾缺血/再灌注损伤 

分 类 号：R692[医药卫生—泌尿科学]