ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Renal Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1606365
This article is part of the Research TopicInnovative Pharmacological Approaches in the Treatment of Urological DisordersView all 7 articles
Selenomethionine Alleviates LPS-Induced Septic Kidney Injury by Regulating Mitochondrial Dynamics Changes
Provisionally accepted
xu zhou1Jiling Zhao2Su Chen1Wusong Cheng1Ya Zhang3Yangang Qu4Xiaohui Hu1
Yong Lan1Qimin Tu5
Jiaxin Hu6*Hongbo Chen1*- 1Department of Urology,Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
- 2Cardiovascular Center,Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
- 3Department of Obstetrics and Gynecology, Enshi Maternal and Child Health Hospital, Enshi, China
- 4Department of Pathology,Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
- 5Cardiothoracic Surgery,Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
- 6Department of Cardiology, Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Wuhan University, Enshi, Hubei, China
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Background: Acute kidney injury (AKI) is a prevalent complication of sepsis, where the inflammatory response plays a crucial role. Selenium exhibits anti-inf lammatory and antioxidant properties, but its impact on sepsis-induced AKI re mains unclear. Methods and Results: In this study, we employed a lipopolysaccharide (LPS)-in duced murine model of sepsis-associated acute kidney injury (SA-AKI) using m ale C57BL/6 mice (8-12 weeks old) to investigate the protective mechanisms o f selenomethionine (SeMet). Mice received weekly oral administration of SeMet (0.375 mg/kg) commencing one week prior to AKI induction. Our results dem onstrated that SeMet treatment significantly attenuated the inflammatory respons e, reduced oxidative stress, and ameliorated renal pathological damage compare d to saline-treated controls. Mechanistic investigations revealed that SeMet mod ulates altered mitochondrial dynamics and suppresses the NF-κB signaling path way, thereby promoting macrophage polarization toward the anti-inflammatory M2 phenotype. Conclusion: These findings collectively demonstrate that SeMet effectively mitig ates inflammation and ameliorates sepsis-induced AKI, suggesting its potential a s a therapeutic candidate for SA-AKI prevention and treatment.
Keywords: Acute Kidney Injury, lipopolysaccharide, Macrophages, Mitochondria, NF-κB
Received: 05 Apr 2025; Accepted: 18 Aug 2025.
Copyright: © 2025 zhou, Zhao, Chen, Cheng, Zhang, Qu, Hu, Lan, Tu, Hu and Chen. 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:
Jiaxin Hu, Department of Cardiology, Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Wuhan University, Enshi, 445000, Hubei, China
Hongbo Chen, Department of Urology,Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
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