臭氧预处理通过调控线粒体裂变与融合平衡减轻肾小管上皮细胞缺氧/复氧损伤

张建伟; 李书强; 马超; 师磊; 袁璞; 刘浩

doi:10.14188/j.1671-8852.2024.0003

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臭氧预处理通过调控线粒体裂变与融合平衡减轻肾小管上皮细胞缺氧/复氧损伤

基础医学研究 | 更新时间：2026-11-05

- 臭氧预处理通过调控线粒体裂变与融合平衡减轻肾小管上皮细胞缺氧/复氧损伤
- Ozone oxidative pretreatment alleviates hypoxia/reoxygenation injury in renal tubular epithelial cells by regulating mitochondrial fission and fusion balance
- 武汉大学学报（医学版） 2025年46卷第5期页码：600-605
- 作者机构：
  
  郑州大学第一附属医院泌尿外科河南郑州 450052
- 作者简介：
  
  张建伟，男，1986—，医学博士，主要从事肾损伤相关疾病研究，E⁃mail:zhangjw429@sina.com
  刘浩，男，1992—，医学博士，主治医师，主要从事肾缺血再灌注损伤研究，E⁃mail：790882508@qq.com
- 基金信息：
  
  国家自然科学青年基金(82300782)
- DOI：10.14188/j.1671-8852.2024.0003
  中图分类号： R692.5
- 收稿：2024-01-02，
  
  纸质出版：2025-05-25
- 稿件说明：
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张建伟,李书强,马超等.臭氧预处理通过调控线粒体裂变与融合平衡减轻肾小管上皮细胞缺氧/复氧损伤[J].武汉大学学报（医学版）,2025,46(05):600-605.

ZHANG Jianwei,LI Shuqiang,MA Chao,et al.Ozone oxidative pretreatment alleviates hypoxia/reoxygenation injury in renal tubular epithelial cells by regulating mitochondrial fission and fusion balance[J].Medical Journal of Wuhan University,2025,46(05):600-605.
张建伟,李书强,马超等.臭氧预处理通过调控线粒体裂变与融合平衡减轻肾小管上皮细胞缺氧/复氧损伤[J].武汉大学学报（医学版）,2025,46(05):600-605. DOI： 10.14188/j.1671-8852.2024.0003.

ZHANG Jianwei,LI Shuqiang,MA Chao,et al.Ozone oxidative pretreatment alleviates hypoxia/reoxygenation injury in renal tubular epithelial cells by regulating mitochondrial fission and fusion balance[J].Medical Journal of Wuhan University,2025,46(05):600-605. DOI： 10.14188/j.1671-8852.2024.0003.

摘要

目的

探究臭氧预处理对肾小管上皮HK2细胞缺氧/复氧损伤的作用及潜在机制。

方法

臭氧预处理HK2细胞后通过缺氧3 h复氧6 h建立缺氧/复氧损伤模型，TUNEL检测细胞凋亡；Western Blot检测Total⁃Drp1、p⁃Drp1 S616、p⁃Drp1 S637、MFN1/MFN2蛋白表达；分离细胞质和线粒体后，Western Blot检测Bax/Bcl2蛋白表达；Mito⁃Tracker染色后利用荧光共聚焦显微镜观察线粒体裂变与融合，并对线粒体数量和纵横比进行统计分析。

结果

臭氧预处理能够明显抑制缺氧/复氧过程细胞凋亡；抑制线粒体Bax蛋白表达并上调线粒体Bcl2蛋白表达。同时臭氧预处理抑制p⁃Drp1 S616蛋白表达，促进MFN1/MFN2蛋白表达；此外能够抑制线粒体裂变，促进线粒体融合。

结论

臭氧预处理能够减轻缺氧/复氧诱导的肾小管上皮细胞凋亡，其潜在机制可能是调控线粒体裂变与融合平衡。

Abstract

Objective

To investigate the effect and potential mechanism of ozone oxidative pretreatment (OzoneOP) on hypoxia/reoxygenation injury in renal tubular epithelial HK2 cells.

Methods

After HK2 cells were treated with OzoneOP

a hypoxia/reoxygenation injury model was established by hypoxia for 3 hours and reoxygenation for 6 hours. Apoptotic cells were measured by TUNEL; Western Blot was used to detect the expression of Total Drp1

p⁃Drp1 S616

p⁃Drp1 S637

and MFN1/MFN2 proteins. The cytoplasm and mitochondria were separated

and Bax/Bcl2 protein expression were detected by using Western Blot. Mito Tracker staining was used to observe mitochondrial fission and fusion under a fluorescence confocal microscope.

Results

OzoneOP inhibited cell apoptosis during hypoxia/reoxygenation processes

suppressed mitochondrial Bax protein expression

and upregulated mitochondrial Bcl2 protein expression. Moreover

ozone pretreatment inhibited the expression of p⁃Drp1 S616 protein and promoted the expression of MFN1/MFN2 protein; In addition

OzoneOP inhibited mitochondrial fission and promoted mitochondrial fusion.

Conclusion

OzoneOP can alleviate hypoxia/reoxygenation⁃induced apoptosis of renal tubular epithelial cells

and its potential mechanism may be to regulate mitochondrial fission and fusion balance.

关键词

Keywords

references

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