核辐射致小鼠急性肾损伤模型的建立及损伤机制的探讨
Establishment of a Mouse Model of Acute Kidney Injury Induced by Nuclear Radiation and Preliminary Study on the Mechanism of Injury
李燕辰 1李建宁 2李峰生 3涂晓文4
作者信息
- 1. 锦州医科大学火箭军特色医学中心研究生培养基地 (北京 100086)
- 2. 宁夏医科大学生化教研室 (银川 750021)
- 3. 火箭军特色医学中心研究部 (北京 100086)
- 4. 火箭军特色医学中心肾脏病科 (北京 100086)
- 折叠
摘要
目的:建立核辐射致小鼠急性肾损伤的模型,利用代谢组学探讨其发病机制.方法:选取C57 小鼠 18 只分对照组和模型组,模型组行15Gy照射辐照6 h、24 h取材.结果:(1)模型组体重下降、肾脏指数增高、血尿素氮及尿微量白蛋白提高,与对照组相比差异均有统计学意义;(2)病理显示辐照后肾组织皮髓质分界不清,伴不同程度的肾小管扩张;(3)代谢组学筛出差异代谢物,并与铁死亡、谷胱甘肽代谢等通路相关.结论:15Gy辐照6 h、24 h可诱导急性肾损伤,并发现与铁死亡相关的代谢物变化.
Abstract
Objective:To establish a mouse model of acute kidney injury induced by nuclear radiation,and to explore its pathogenesis by Metabonomics.Methods:Eighteen C57 mice were divided into control group and model group.The model group was irradiated with 15Gy.The samples were taken at 6 h and 24 h after irradiation.Results:(1)Compared with the control group,the body weight decreased,renal index increased,blood urea nitrogen and urine microalbumin increased in the model group;(2)The re-nal cortex and medulla were poorly demarcated and the renal tubules were dilated;(3)Metabolomics has identified a variety of differ-ent metabolites that are associated with pathways such as Ferroptosis and Glutathione metabolism.Conclusion:15Gy irradiation for 6 h and 24 h could induce AKI,and the metabolite changes associated with Ferroptosis were found.
关键词
核辐射/急性肾损伤/代谢组学/铁死亡Key words
Nuclear radiation/AKI/Metabolomics/Ferroptosis引用本文复制引用
出版年
2024
NETL
NSTL
万方数据