Evidence map›Paper›PMID 42241031›Full record

ArticleRedox report : communications in free radical research2026

Uric acid alleviates the inflammatory response in LPS-induced BV2 cells and MPTP-induced PD mice by resisting ferroptosis through the Nrf2 signalling pathway.

Dongmei Zhou, Tian Xiong, Bing Yang, Fanjie Liu, Xianglai Mo, Ting Chen, Peipei Lu, Xinghuan Liang, Li Li, Yingfen Qin and 3 more

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Article in Redox report : communications in free radical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

13 authors.

Dongmei ZhouDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Tian XiongGuangxi Key Laboratory of Precision Medicine in Cardio-Cerebrovascular Diseases Control and Prevention, Guangxi Clinical Research Center for Cardio-Cerebrovascular Diseases, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Bing YangDepartment of Gastrointestinal Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Fanjie LiuDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Xianglai MoDepartment of Geriatric Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Ting ChenDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Peipei LuDepartment of Geriatric Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Xinghuan LiangDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Li LiDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Yingfen QinDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Decheng LuDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Feng HuangGuangxi Key Laboratory of Precision Medicine in Cardio-Cerebrovascular Diseases Control and Prevention, Guangxi Clinical Research Center for Cardio-Cerebrovascular Diseases, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Xi YangDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation, oxidative stress, and ferroptosis are implicated in Parkinson' s disease (PD) pathogenesis. Epidemiological studies suggest that elevated uric acid (UA) levels may reduce PD risk, but the precise molecular mechanisms involved remain unclear. In this study, we investigated the effects of UA in lipopolysaccharide (LPS) or MPP+-stimulated BV2 microglia and MPTP-induced PD mouse models.

methodsBV2 cells are recognized as a standardized and reproducible neural inflammatory cell model for mechanism exploration. The anti-ferroptosis and anti-inflammatory effects of UA were assessed in LPS or MPP+ stimulated BV2 microglia and in an MPTP-induced PD mouse model. Western blot, qPCR, ELISA, and immunofluorescence were used to analyse the expression of inflammasome-related markers. ROS, MDA, GSH, and Fe²⁺ levels were measured using testing kits, while mitochondrial ultrastructure was evaluated through transmission electron microscopy. PD-related markers were assessed by ethology and immunohistochemistry. The Nrf2 inhibitor ML385 was employed to validate pathway specificity.

resultsWe found that UA treatment reduced the expression of proinflammatory cytokines (TNF-

conclusionUA alleviates ferroptosis and neuroinflammation in LPS or MPP+ stimulated BV2 microglia and MPTP-induced PD mouse models through the activation of the Nrf2 signalling pathway.

Indexed as

FerroptosisInflammationNF-E2-Related Factor 2Parkinson DiseaseUric AcidAnimalsCell LineDisease Models, AnimalLipopolysaccharidesMaleMiceMice, Inbred C57BLMicrogliaOxidative StressReactive Oxygen SpeciesSignal TransductionLipopolysaccharidesNfe2l2 protein, mouseNF-E2-Related Factor 2Reactive Oxygen SpeciesUric AcidferroptosisinflammationNrf2Parkinson’s diseaseUric acid

Identifiers

PMID42241031
PMCPMC13237794

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