ORIGINAL RESEARCH article
Front. Nutr.
Sec. Nutrition and Metabolism
Volume 12 - 2025 | doi: 10.3389/fnut.2025.1677560
This article is part of the Research TopicRegulation and Mechanism of Plant Metabolites on HyperuricemiaView all 5 articles
Aloe-emodin attenuates hyperuricemia-induced renal injury in mice by mitigating inflammation and oxidative stress
Provisionally accepted
Shengfeng Wang1
Quanfeng Zhu2
Chengcheng Zhang3Shuang Hu4
Daqun Liu3Jiawen Yu2Xiao Liu2Yan Chen1*
Guojun Jiang2*- 1Zhejiang University of Technology, Hangzhou, China
- 2Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, China
- 3Zhejiang Academy of Agricultural Sciences, Hangzhou, China
- 4Hangzhou Normal University, Hangzhou, China
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Background: Aloe-emodin (AOE), the principal anthraquinone constituent derived from aloe and rhubarb, exhibits antioxidant and anti-inflammatory properties, suggesting its therapeutic potential against hyperuricemia (HUA) and associated renal injury. Here, we investigated the potential of AOE in mitigating HUA and related kidney damage, with a focus on its underlying biological mechanisms. Methods: A HUA mouse model was established by oral gavage of potassium oxonate (PO, 1.5 g/kg) and adenine (Ad, 0.1 g/kg). Serum uric acid (UA) levels, kidney function indicators, histological changes, inflammatory response, and oxidative stress state were assessed to evaluate the urate-lowering and kidney-protective roles of AOE. Furthermore, transcriptomic profiling and RT-qPCR analysis were employed to investigate how AOE contributes to UA reduction and renal protection. Results: AOE lowered serum UA levels and inhibited xanthine oxidase and adenosine deaminase activity. Moreover, AOE improved kidney function indicators (reflected by reductions in serum creatinine and blood urea nitrogen levels), restored the integrity of renal tissue structure, and mitigated inflammation and oxidative stress in HUA-exposed animals. Transcriptomic analysis revealed 2307 differentially expressed key genes associated with AOE against HUA in kidney. Furthermore, AOE downregulated p65/RelA and NF-κB1/p50 transcript levels, while increasing PPARα, PPARγ, and CPT2 expression. Conclusions: AOE effectively lowered serum UA levels, and exhibited renal protection in the PO/Ad-induced HUA mouse model by dampening inflammatory signaling and restoring redox equilibrium, likely through the PPAR and NF-κB pathways. This study demonstrated that AOE is a promising natural candidate with a desirable safety profile for treating HUA and renal injury, and more experimental validation are needed in the future.
Keywords: Aloe-emodin, Hyperuricemia, renal injury, Oxidative Stress, Inflammatory Response, PPAR/NF-κB signaling
Received: 01 Aug 2025; Accepted: 24 Sep 2025.
Copyright: © 2025 Wang, Zhu, Zhang, Hu, Liu, Yu, Liu, Chen and Jiang. 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:
Yan Chen, chenyan2008@zjut.edu.cn
Guojun Jiang, jguojun999@hznu.edu.cn
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