Evidence map›Paper›PMID 35080474›Full record

ArticleRedox report : communications in free radical research2022

Chemopreventive and hepatoprotective effects of genistein via inhibition of oxidative stress and the versican/PDGF/PKC signaling pathway in experimentally induced hepatocellular carcinoma in rats by thioacetamide.

Yousra M El-Far, Ahmed E Khodir, Ziad A Emarah, Mohamed A Ebrahim, Mohammed M H Al-Gayyar

Open access · goldAbstract read
In one paragraph

Article in Redox report : communications in free radical research, 2022. 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
3.0field-weighted citation impact, top 8% 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, 35 citations in OpenAlex.

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  20. Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022
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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 2 countries.

Yousra M El-FarFaculty of Pharmacy, Department of Biochemistry, Mansoura University, Mansoura, Egypt.
Ahmed E KhodirFaculty of Pharmacy, Department of Pharmacology, Horus University in Egypt, New Damietta, Egypt.
Ziad A EmarahFaculty of Medicine, Department of Internal Medicine, Mansoura University, Mansoura, Egypt.
Mohamed A EbrahimDepartment of Medical Oncology, Oncology Center, Mansoura University, Mansoura, Egypt.
Mohammed M H Al-GayyarFaculty of Pharmacy, Department of Biochemistry, Mansoura University, Mansoura, Egypt.ORCID 0000-0003-4777-3919
Mansoura University · EGDamietta University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGenistein is a recognized isoflavone present in soybeans with antioxidant, anti-inflammatory, antiangiogenic and antitumor activities. This study aimed to test ability of genistein in modulating versican/platelet derived growth factor (PDGF) axis in HCC.

methodsHCC was experimentally induced in male Sprague-Dawley rats then treated with 25 or 75 mg/kg genistein. Antioxidant activities of genistein was assessed by measuring the gene expression of Nrf2 and the hepatic levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione. Expression of versican, PDGF, protein kinase C (PKC) and ERK-1 protein was assessed by Western blotting and immunostaining.

resultsHCC induced an elevation in oxidative stress, PDGF, versican, PKC and ERK protein expression levels. Genistein significantly reduced an HCC-induced increase in oxidative stress. Moreover, genistein dose-dependently reduced HCC-induced elevation of PDGF, versican, PKC and ERK protein expression levels. Moreover, genistein helped retain a normal hepatocyte structure and reduced fibrous tissue deposition, especially in high dose.

conclusionsGenistein exerted antitumor and antioxidant effects and therefore suppress HCC development via inhibition of the PDGF/versican bidirectional axis, suppressing both ERK1 and PKC as downstream regulators. Therefore, genistein is a potential novel therapeutic candidate for improving the outcome of patients with HCC.

Indexed as

Carcinoma, HepatocellularGenisteinLiver NeoplasmsOxidative StressSignal TransductionAnimalsMalePlatelet-Derived Growth FactorRatsRats, Sprague-DawleyThioacetamideVersicansGenisteinPlatelet-Derived Growth FactorThioacetamideVersicansERKgenisteinhepatocellular carcinomaNrf2platelet-derived growth factorprotein kinase Cversican

Identifiers

PMID35080474
PMCPMC8794077
OpenAlexW4210555628

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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.