Evidence map›Paper›PMID 30225683›Full record

ArticleJournal of molecular histology2018

Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction.

Mei Yang, Jun Xiong, Qiang Zou, Dan-Dan Wang, Cong-Xin Huang

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
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

35 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Anticancer Activity of Ether Derivatives of Chrysin.Molecules (Basel, Switzerland) · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Chrysin protects cardiac H9c2 cells against HMolecular and cellular biochemistry · 2023
    Article
  14. Review
  15. Article
  16. Frontiers in pharmacology · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Mei YangDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, People's Republic of China.
Jun XiongDepartment of Emergency, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Qiang ZouDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, People's Republic of China.
Dan-Dan WangDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, People's Republic of China.
Cong-Xin HuangDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, People's Republic of China. huangcongxin@vip.163.com.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

Fundamental Research Funds for the Central Universities 2018413000185
6 · The paper itself

Abstract

Interstitial fibrosis after acute myocardial infarction (MI) leads to cardiac structural remodeling and dysfunction. The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. This study was designed to investigate the effect and mechanism of chrysin on myocardial fibrosis. A rat MI model was created by ligating the left coronary artery. The rats with MI were treated with chrysin (40 mg/kg/day) or 0.5% carboxymethylcellulose sodium by intragastric administration for 4 weeks after operation. The effect of chrysin on cardiac fibroblasts (CFs) were also assessed in vitro. Echocardiography showed that cardiac function was significantly improved after chrysin treatment. Chrysin reduced the levels of MDA and SOD and GSH-Px in myocardial tissue. Chrysin attenuated the interstitial and perivascular fibrosis and the expression of collagenlin the peri-infarcted zone and remarkably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. Chrysin up-regulated PPAR-γ and inhibited the nuclear factor-kappa B (NF-κB) pathway by suppressing inhibitor kappa B kinase β phosphorylation. Immunohistochemistry analysis and PCR detected downregulated expression of AP-1 after chrysin treatment. Chrysin also markedly reduced the increased α-SMA, typeland type III collagen expression of CFs mediated by AngII in vitro. In conclusion, chrysin has an antifibrosis cardioprotective effect on the infarct peripheral zone after MI. The underlined mechanism may be the up-regulation of PPAR-γ and inhibition of the NF-κB and AP1 pathway.

Indexed as

AnimalsDisease Models, AnimalFibroblastsFibrosisFlavonoidsHeartMyocardial InfarctionNF-kappa BPPAR gammaRatsTranscription Factor AP-1Up-RegulationchrysinFlavonoidsNF-kappa BPPAR gammaTranscription Factor AP-1AP1ChrysinInterstitial fibrosisMyocardial infarctionNF-κBPPAR-γ

Identifiers

PMID30225683
OpenAlexW2890509961

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.