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ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Integrative and Regenerative Pharmacology
Volume 15 - 2024 |
doi: 10.3389/fphar.2024.1438127
This article is part of the Research Topic Recent Advances in the Management of Crush Syndrome: From Bench to Bedside View all 4 articles
Paving the Way Ahead: Protocol Optimization of Mouse Models in Crush Syndrome Related Acute Kidney Injury Research
Provisionally accepted- Tianjin University, Tianjin, China
Backgrounds: Crush syndrome (CS) is the leading cause of death after earthquakes, second only to direct trauma. Acute kidney injury (AKI) is the most severe complication of CS. Research based on the CS-AKI mouse model and kidney function assessment by glomerular filtration rate (GFR) helps to elucidate the pathogenesis of CS-AKI, which contributes to effective treatment measures.Methods: Mice were modeled by the multi-channel small animal crushing platform. We set up different CS-AKI modeling parameters by applying different crushing weights (0.5 kg, 1.0 kg, 1.5 kg), crushing durations (6 h, 12 h, 16 h), and decompression durations (6 h, 12 h, 24 h). The GFR, serum creatinine (SCr), blood urea nitrogen (BUN), kidney tissue Kim-1 mRNA and Ngal mRNA expression levels, and HE staining were examined to evaluate the results of different protocols.The results showed that with the crushing weight increased, the kidney function assessment's gold standard GFR significantly decreased, and the levels of SCr and BUN increased.Meantime, the higher extension of inflammatory cell infiltration in the kidney was found with the longer crushing durations. The degree of kidney injury continued to worsen with the duration of decompression, indicating severe damage after reperfusion, which was associated with tubular injury and a sustained elevation of the inflammatory state.We successfully constructed CS-AKI mouse models with different severities under the above parameters. Applying 1.5 kg for 16 h and then decompressing for 24 h induced severe AKI. These findings provide clues for further exploration of the mechanism and treatment of traumatic AKI.
Keywords: Crush Syndrome, Acute Kidney Injury, mouse model, GFR, Rhabdomyolysis
Received: 25 May 2024; Accepted: 20 Sep 2024.
Copyright: © 2024 Qiao, Wang, Li, Han, Chen, Zhang, Bao, Hao, Hou, Duan, Saeed, Li and Gong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Xinyue Wang, Tianjin University, Tianjin, China
Zizheng Li, Tianjin University, Tianjin, China
Lu Han, Tianjin University, Tianjin, China
Xin Chen, Tianjin University, Tianjin, China
Li Zhang, Tianjin University, Tianjin, China
Fengjiao Bao, Tianjin University, Tianjin, China
Herui Hao, Tianjin University, Tianjin, China
Yingjie Hou, Tianjin University, Tianjin, China
Xiaohong Duan, Tianjin University, Tianjin, China
Ning Li, Tianjin University, Tianjin, China
Yanhua Gong, Tianjin University, Tianjin, China
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