Evidence map›Paper›PMID 41045342›Full record

ArticleInflammopharmacology2025

Kaempferol prevents Nrf2 from ubiquitin-mediated proteolysis to mitigate both NLRP3 inflammation and oxidative stress: implications for alleviating DSS-induced colitis in mice.

Wentian Hua, Minrui Li, Ziwei Yan, Yingchao Wang, Xiang Zhou, Zhiwen Fu, Yi Wang, Shujing Zhang, Jing Qian

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Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Black tea-processedFrontiers in nutrition · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Wentian HuaPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Minrui LiPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Ziwei YanPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Yingchao WangPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Xiang ZhouZhejiang Key Laboratory of Major TCM Cultivation and TCM Innovation, Hangzhou, 310052, China.
Zhiwen FuJiangxi Conba Traditional Chinese Medicine Co.,Ltd., Shangrao, 334400, China.
Yi WangPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Shujing ZhangPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China. 11619025@zju.edu.cn.
Jing QianPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China. jingqian@zju.edu.cn.ORCID http://orcid.org/0000-0002-1642-9202

Funding

Key Technologies Research and Development Program 2023YFC3502801Medical Science and Technology Project of Zhejiang Province 2024ZL343National Natural Science Foundation of China 82304755
6 · The paper itself

Abstract

backgroundActivation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and oxidative stress are key pathological hallmarks of inflammatory bowel disease (IBD) and represent novel targets for therapeutic intervention. The therapeutic potential of the naturally occurring flavonoid kaempferol (KAE) in IBD, along with its underlying molecular mechanisms, remains incompletely understood.

methodsWe established dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced systemic inflammation mouse models. KAE was administered as an intervention. In vitro, peritoneal macrophages (PMs) were stimulated to activate the NLRP3 inflammasome. We comprehensively evaluated the effects of KAE on interleukin-1β (IL-1β) release, NLRP3 inflammasome assembly, and mitochondrial reactive oxygen species (mt-ROS) production. Additionally, we assessed its impact on the Keap1-Nrf2 pathway. Molecular docking and ubiquitin-dependent degradation assays were conducted to confirm Nrf2 as a direct target of KAE.

resultsKAE significantly attenuated colitis development, marked by reduced NLRP3 expression and enhanced Nrf2 activation. It inhibited both the priming and assembly phases of NLRP3 inflammasome activation. Notably, Nrf2 inhibition completely abolished KAE-mediated removal of mt-ROS and downstream suppression of NLRP3 inflammasome activation. Mechanistically, KAE prevented Nrf2 proteolysis by directly binding to Arg415 of Keap1.

conclusionsOur findings demonstrate that KAE acts as an mt-ROS scavenger to protect against inflammatory pyroptosis, offering novel mechanistic insights and a promising therapeutic strategy for colitis treatment.

Indexed as

ColitisKaempferolsNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressAnimalsDextran SulfateDisease Models, AnimalInflammasomesInflammationKelch-Like ECH-Associated Protein 1Macrophages, PeritonealMaleMiceMice, Inbred C57BLMolecular Docking SimulationDextran SulfateInflammasomeskaempferolKaempferolsKelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesUbiquitinColitisKaempferolNLRP3 inflammasomeNrf2Oxidative stress

Identifiers

PMID41045342

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.