Evidence map›Paper›PMID 31067255›Full record

ArticlePloS one2019

Regression of fibrosis by cilostazol in a rat model of thioacetamide-induced liver fibrosis: Up regulation of hepatic cAMP, and modulation of inflammatory, oxidative stress and apoptotic biomarkers.

Sally A El Awdan, Rehab F Abdel Rahman, Heba M Ibrahim, Rehab R Hegazy, Salma A El Marasy, Manal Badawi, Mahmoud S Arbid

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 55 citations in OpenAlex.

  1. Therapeutic effects of alprostadil on CClMolecular and cellular biochemistry · 2026
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  10. Targeting cAMP signaling and phosphodiesterase 4 for liver disease treatment.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2024
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  16. Cilostazol Attenuates AngII-Induced Cardiac Fibrosis in apoE Deficient Mice.International journal of molecular sciences · 2022
    Article
  17. Review
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  19. 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

7 authors at 1 institution in 1 country.

Sally A El AwdanPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.
Rehab F Abdel RahmanPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.
Heba M IbrahimPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.
Rehab R HegazyPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.ORCID 0000-0002-2586-2104
Salma A El MarasyPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.ORCID 0000-0002-8730-0297
Manal BadawiPathology Department, Medical Division, National Research Centre, Giza, Egypt.
Mahmoud S ArbidPharmacology Department, Medical Division, National Research Centre, Giza, Egypt.
National Research Centre · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In liver fibrosis, conversion of fibroblasts to profibrogenic myofibroblasts significantly drives the development of the disease. A crucial role of cyclic adenosine monophosphate (cAMP) in regulation of fibroblast function has been reported. Increase in cAMP levels has been found to decrease fibroblast proliferation, inhibit their conversion to myofibroblast, and stimulate their death. cAMP is generated by adenyl cyclase (AC), and degraded by cyclic nucleotide phosphodiesterase (PDE). In this study, the antifibrotic effect of a PDE inhibitor, cilostazol (Cilo), on a rat model of liver fibrosis induced by thioacetamide (TAA) was investigated. Four groups of rats were used; the first group received the vehicles and served as the normal control group, while liver fibrosis was induced in the other groups using (TAA, 200 mg/kg/biweekly for 8 successive weeks, ip). The last two groups were treated with Cilo (50 and 100 mg/kg/day, po, respectively). Induction of liver fibrosis in TAA-treated rats was observed as evidenced by the biochemical and histopathological findings. On the other hand, a potent antifibrotic effect was observed in the groups treated with Cilo, with preference to the higher dose. In these groups, a significant increase in the liver content of cAMP was demonstrated that was accompanied by reduction in the hepatic expression of key fibrogenic cytokines, growth factors, and inflammatory biomarkers, including interleukin-6, tumor necrosis factor-alpha, nuclear factor kappa B, and transforming growth factor-beta as compared to TAA group. Moreover, amelioration of TAA-induced oxidative stress and apoptosis in the liver has been observed. These findings reveal the antifibrotic effect of Cilo against TAA-induced liver fibrosis in rats, and suggest regulation of cAMP pathway, together with the modulation of oxidative stress, inflammation, and apoptosis as mechanistic cassette underlines this effect.

Indexed as

AnimalsApoptosisBiomarkersCilostazolCyclic AMPInflammationLiverLiver CirrhosisOxidative StressRatsThioacetamideUp-RegulationBiomarkersCilostazolCyclic AMPThioacetamide

Identifiers

PMID31067255
PMCPMC6505801
OpenAlexW2943902917

What Socratic holds

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LicenceCC BY
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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 Socratic graph.