Evidence map›Paper›PMID 22722906›Full record

ArticleJournal of gastroenterology2013

Butein inhibits ethanol-induced activation of liver stellate cells through TGF-β, NFκB, p38, and JNK signaling pathways and inhibition of oxidative stress.

Agnieszka Szuster-Ciesielska, Magdalena Mizerska-Dudka, Jadwiga Daniluk, Martyna Kandefer-Szerszeń

Open access · hybridAbstract read
In one paragraph

Article in Journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-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

30 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
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  3. Review
  4. Saffron andWorld journal of gastroenterology · 2025
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  8. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
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  18. Apoptotic effects of hsian-tsao (Food science & nutrition · 2019
    Article
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  20. Açaí (Experimental and therapeutic medicine · 2018
    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

4 authors at 2 institutions in 1 country.

Agnieszka Szuster-CiesielskaDepartment of Virology and Immunology, Maria Curie-Skłodowska University, Akademicka 19, 20-033, Lublin, Poland. szustera@hektor.umcs.lublin.pl
Magdalena Mizerska-Dudka
Jadwiga Daniluk
Martyna Kandefer-Szerszeń
Maria Curie-Skłodowska University · PLMedical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundButein has been reported to prevent and partly reverse liver fibrosis in vivo; however, the mechanisms of its action are poorly understood. We, therefore, aimed to determine the antifibrotic potential of butein.

methodsWe assessed the influence of the incubation of hepatic stellate cells (HSCs) and hepatoma cells (HepG2) with butein on sensitivity to ethanol- or acetaldehyde-induced toxicity; the production of reactive oxygen species (ROS); the expression of markers of HSC activation, including smooth muscle α-actin (α-SMA) and procollagen I; and the production of transforming growth factor-β1 (TGF-β1), metalloproteinases-2 and -13 (MMP-2and MMP-13), and tissue inhibitors of metalloproteinases (TIMPs). The influence of butein on intracellular signals in HSCs; i.e., nuclear factor-κB (NFκB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) induced by ethanol was estimated.

resultsButein protected HSCs and HepG2 cells against ethanol toxicity by the inhibition of ethanol- or acetaldehyde-induced production of ROS when cells were incubated separately or in co-cultures; butein also inhibited HSC activation measured as the production of α-SMA and procollagen I. As well, butein downregulated ethanol- or acetaldehyde-induced HSC migration and the production of TGF-β, TIMP-1, and TIMP-2; decreased the activity of MMP-2; and increased the activity of MMP-13. In ethanol-induced HSCs, butein inhibited the activation of the p38 MAPK and JNK transduction pathways as well as significantly inhibiting the phosphorylation of NF κB inhibitor (IκB) and Smad3.

conclusionsThe results indicated that butein inhibited ethanol- and acetaldehyde-induced activation of HSCs at different levels, acting as an antioxidant and inhibitor of ethanol-induced MAPK, TGF-β, and NFκB/IκB transduction signaling; this result makes butein a promising agent for antifibrotic therapies.

Indexed as

AcetaldehydeActinsAnimalsAntioxidantsCell DeathCells, CulturedChalconesCoculture TechniquesCollagen Type IDrug Evaluation, PreclinicalEthanolHepatic Stellate CellsHep G2 CellsHumansMAP Kinase Kinase 4NF-kappa BAcetaldehydeActa2 protein, ratActinsAntioxidantsbuteinChalconesCollagen Type IEthanolMAP Kinase Kinase 4NF-kappa Bp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTransforming Growth Factor beta

Identifiers

PMID22722906
PMCPMC3575555
OpenAlexW1991047372

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.