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Peer-reviewedCC BY 4.0Frontiers in Immunology

Evodiamine attenuates hyperuricemia-associated gouty arthritis and renal injury through urate-inflammatory axis modulation

  • Yu Mou1
  • Wenhao Liao2
  • Qun Niu1
  • Xue Zhan1
  • Tianxin Zhang3
  • YuChen Li4
  • Hong Che1
  • Peijia Liu1
  • Xiangdong Yang1
  • Jianyuan Tang5,6
  • Zhilei Wang6
6 affiliations
  1. 1Department of Hematology, Hospital of Chengdu University of Traditional Chinese Medicine
  2. 2Department of Nephrology, the Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University)
  3. 3Department of Laboratory Medicine, the Third Affiliated Hospital of Zhengzhou University, Zhengzhou Key Laboratory for In Vitro Diagnosis of Hypertensive Disorders of Pregnancy
  4. 4Department of Laboratory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine
  5. 5Sichuan Academy of Chinese Medicine Sciences
  6. 6TCM Prevention and Treatment of Metabolic and Chronic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine
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Abstract

Background: Therapeutic options for hyperuricemia (HUA) and its complications remain inadequate, particularly when gouty arthritis (GA) and hyperuricemic nephropathy (HN) coexist. Agents with combined urate-lowering, anti-inflammatory, and renoprotective effects are therefore needed. Evodiamine (EVO), a major alkaloid from Evodia rutaecarpa , exhibits anti-inflammatory and analgesic activities, but its role in HUA-related disorders has not been fully defined.

Study design and methods: We examined the effects of Evodia rutaecarpa water extract (ERWE) and EVO in experimental models of HUA, HN, and GA.

Results: In the HUA model, ERWE reduced plasma UA levels and increased urinary UA concentration, accompanied by reductions in ALT, AST, and selected inflammatory measurements. Metabolomic profiling indicated that these effects were associated with alterations in pyrimidine metabolism, α-linolenic acid metabolism, and butyrate-related pathways. In the HN model, EVO lowered serum UA and creatinine levels, improved renal pathology, and reduced renal URAT1 and GLUT9 expression. EVO also suppressed NLRP3/caspase-1/IL-1β signaling and reduced the expression of fibrosis-related markers, including α-SMA, COL1A1, and TIMP1. In the GA model, EVO alleviated monosodium urate (MSU)-induced ankle swelling, leukocyte infiltration, and inflammatory mediator production, including IL-1β, TNF-α, and MPO, while inhibiting NLRP3 inflammasome activation.

Conclusion: ERWE and the alkaloid EVO showed significant protective effects in experimental HUA-related disorders. EVO, in particular, exerted urate-lowering, renoprotective, and anti-inflammatory activities, possibly through regulation of urate transporters and NLRP3 inflammasome signaling.

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Cite

BibTeXRIS
BibTeX
@article{mou2026evodiamine,
  title = {{Evodiamine attenuates hyperuricemia-associated gouty arthritis and renal injury through urate-inflammatory axis modulation}},
  author = {Yu Mou and Wenhao Liao and Qun Niu and Xue Zhan and Tianxin Zhang and YuChen Li and Hong Che and Peijia Liu and Xiangdong Yang and Jianyuan Tang and Zhilei Wang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1932250},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1932250/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Evodiamine attenuates hyperuricemia-associated gouty arthritis and renal injury through urate-inflammatory axis modulation
AU  - Yu Mou
AU  - Wenhao Liao
AU  - Qun Niu
AU  - Xue Zhan
AU  - Tianxin Zhang
AU  - YuChen Li
AU  - Hong Che
AU  - Peijia Liu
AU  - Xiangdong Yang
AU  - Jianyuan Tang
AU  - Zhilei Wang
PY  - 2026
DA  - 2026/10/22
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1932250
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1932250/full
AB  - Background: Therapeutic options for hyperuricemia (HUA) and its complications remain inadequate, particularly when gouty arthritis (GA) and hyperuricemic nephropathy (HN) coexist. Agents with combined urate-lowering, anti-inflammatory, and renoprotective effects are therefore needed. Evodiamine (EVO), a major alkaloid from Evodia rutaecarpa , exhibits anti-inflammatory and analgesic activities, but its role in HUA-related disorders has not been fully defined.  Study design and methods: We examined the effects of Evodia rutaecarpa water extract (ERWE) and EVO in experimental models of HUA, HN, and GA.  Results: In the HUA model, ERWE reduced plasma UA levels and increased urinary UA concentration, accompanied by reductions in ALT, AST, and selected inflammatory measurements. Metabolomic profiling indicated that these effects were associated with alterations in pyrimidine metabolism, α-linolenic acid metabolism, and butyrate-related pathways. In the HN model, EVO lowered serum UA and creatinine levels, improved renal pathology, and reduced renal URAT1 and GLUT9 expression. EVO also suppressed NLRP3/caspase-1/IL-1β signaling and reduced the expression of fibrosis-related markers, including α-SMA, COL1A1, and TIMP1. In the GA model, EVO alleviated monosodium urate (MSU)-induced ankle swelling, leukocyte infiltration, and inflammatory mediator production, including IL-1β, TNF-α, and MPO, while inhibiting NLRP3 inflammasome activation.  Conclusion: ERWE and the alkaloid EVO showed significant protective effects in experimental HUA-related disorders. EVO, in particular, exerted urate-lowering, renoprotective, and anti-inflammatory activities, possibly through regulation of urate transporters and NLRP3 inflammasome signaling.
SN  - 1664-3224
ER  -