Evidence map›Paper›PMID 40285837›Full record

ArticleMolecular biology reports2025

Chrysin improves endothelial inflammation via the NFAT pathway in Kawasaki disease.

Jin Ma, Yan Li, Yunjia Tang, Guanghui Qian, Haitao Lv, Xiudao Song, Ying Liu

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Article in Molecular biology reports, 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.

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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

7 authors.

Jin MaDepartment of Pharmacy, Children's Hospital of Soochow University, 215025, Suzhou, China.
Yan LiDepartment of Pediatrics, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, China, 215009.
Yunjia TangDepartment of Cardiology, Children's Hospital of Soochow University, 215025, Suzhou, China.
Guanghui QianInstitute of Pediatric Research, Children's Hospital of Soochow University, No. 92 Zhongnan Street, Jiangsu, 215025, Suzhou, China.
Haitao LvDepartment of Cardiology, Children's Hospital of Soochow University, 215025, Suzhou, China.
Xiudao SongTraditional Chinese Medicine Technology Transfer Center, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, No. 18 Yangsu Street, Jiangsu, 215009, Suzhou, China. fsyy00530@njucm.edu.cn.
Ying LiuInstitute of Pediatric Research, Children's Hospital of Soochow University, No. 92 Zhongnan Street, Jiangsu, 215025, Suzhou, China. d201077400@alumni.hust.edu.cn.

Funding

National Natural Science Foundation of China 82270529
6 · The paper itself

Abstract

backgroundThe purpose of this study was to evaluate the therapeutic effects of Chrysin on endothelial inflammation in a KD mouse model and to elucidate the molecular mechanisms underlying these effects, with a particular focus on the NFAT2 signaling pathway. METHODS AND

resultsIn vivo, a KD mouse model was used to assess the effects of Chrysin on coronary artery inflammation. Histological analysis, immunohistochemistry, and cytokine profiling were performed to evaluate inflammatory cell infiltration, structural changes in the arteries, and modulation of key inflammatory cytokines. In vitro, TNFα-stimulated HCAECs were used to examine the protective effects of Chrysin on endothelial injury, including cytokine secretion and adhesion molecule expression. Mechanistic studies were conducted to explore the role of the NFAT2 signaling pathway in mediating Chrysin's effects, utilizing molecular docking analysis and Western blotting. In vivo, Chrysin treatment significantly alleviated coronary artery inflammation in the KD mouse model. Histological analysis revealed reduced inflammatory cell infiltration and improved elastin fiber structure. Cytokine analysis showed that Chrysin attenuated the elevated levels of IL-6, IL-17, TNFα, and MCP-1 in KD mice. In vitro, Chrysin reduced TNFα-induced endothelial injury, as evidenced by decreased secretion of IL-6, IL-8, IL-23, ICAM-1 and VCAM-1 in HCAECs. Mechanistic investigations revealed that Chrysin's effects on endothelial inflammation were mediated through the NFAT2 signaling pathway, rather than the upstream PLCγ1 pathway, as confirmed by molecular docking and Western blotting. Inhibition of PLCγ1 did not alter the protective effects of Chrysin, suggesting that its action is primarily through NFAT2.

conclusionsThis study provides the first evidence that Chrysin significantly reduces endothelial inflammation and vascular injury in KD. The observed anti-inflammatory effects are mediated through the NFAT2 signaling pathway, highlighting the potential of Chrysin as a therapeutic agent for managing KD and its associated vascular complications.

Indexed as

FlavonoidsMucocutaneous Lymph Node SyndromeNFATC Transcription FactorsAnimalsCoronary VesselsCytokinesDisease Models, AnimalEndothelial CellsEndothelium, VascularHumansInflammationMaleMiceMolecular Docking SimulationSignal TransductionTumor Necrosis Factor-alphachrysinCytokinesFlavonoidsNFATC Transcription FactorsTumor Necrosis Factor-alphaEndothelial cellsKawasaki diseaseNFAT2PLCγ1

Identifiers

PMID40285837

What Socratic holds

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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 Socratic graph.