Evidence map›Paper›PMID 30066878›Full record

ArticleMolecular medicine reports2018

Emodin alleviates CCl4‑induced liver fibrosis by suppressing epithelial‑mesenchymal transition and transforming growth factor‑β1 in rats.

Feng Liu, Jing Zhang, Jianmin Qian, Gang Wu, Zhenyu Ma

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  4. Pharmaceuticals (Basel, Switzerland) · 2024
    Review
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  7. Article
  8. Article
  9. Nutrients · 2022
    Article
  10. Role and Mechanism of Epithelial-Mesenchymal Transition Mediated by Inflammatory Stress-Induced TGF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  11. Review
  12. Review
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  15. Article
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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

5 authors at 2 institutions in 1 country.

Feng LiuDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Jing ZhangDepartment of Nursing Center, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Jianmin QianDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Gang WuDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Zhenyu MaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Huashan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is a chronic disease that exhibits a complicated pathophysiology. It is characterized by the deposition of the extracellular matrix. Emodin, an active constituent isolated from rhubarb, has antibacterial, immunosuppressive and anti‑inflammatory effects. In the present study, the mechanism through which emodin alleviates liver fibrosis in rats was investigated. A rat model of liver fibrosis was generated by administering CCl4 via subcutaneous injection twice a week for 12 weeks. Emodin or sodium carboxymethylcellulose (CMC), as the vehicle, were intragastrically administered daily. After 12 weeks, the liver function index was examined by blood analysis, histopathological scores of fibrosis was determined by hematoxylin and eosin staining and level of collagen deposition was examined by Masson staining. In addition, protein and RNA samples were collected for further analysis. The results of the present study revealed that emodin significantly reduced the liver function index and level of collagen deposition in a dose‑dependent manner. Furthermore, emodin reduced the expression of transforming growth factor‑β1 (TGF‑β1) and the phosphorylation levels of mothers against decapentaplegic homolog 2/3, and inhibited the CCl4‑induced downregulation of E‑cadherin and upregulation of the mesenchymal markers, fibronectin and vimentin. The expression levels of TGF‑β1, Snail family transcriptional repressor (Snail) 2, Snail, twist‑related protein 1 and zinc finger E‑box‑binding homeobox (ZEB)1 and 2 mRNA were significantly decreased in emodin‑treated groups compared with the untreated control. Collectively, the results of the present study suggested that emodin may exert antifibrotic effects via the suppression of TGF‑β1 signaling and epithelial‑mesenchymal transition.

Indexed as

AnimalsBiomarkersCarbon TetrachlorideCollagenDisease Models, AnimalEmodinEpithelial-Mesenchymal TransitionGene ExpressionLiver CirrhosisLiver Function TestsMaleProtein Kinase InhibitorsRatsSeverity of Illness IndexSmad2 ProteinSmad3 ProteinBiomarkersCarbon TetrachlorideCollagenEmodinProtein Kinase InhibitorsSmad2 ProteinSmad3 ProteinTransforming Growth Factor beta1

Identifiers

PMID30066878
PMCPMC6102702
OpenAlexW2883528230

What OpenQuestion holds

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Registered trials

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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.