Evidence map›Paper›PMID 22535497›Full record

ArticleInflammation2012

Allopurinol ameliorates thioacetamide-induced acute liver failure by regulating cellular redox-sensitive transcription factors in rats.

Ulvi Demirel, Mehmet Yalniz, Cem Aygün, Cemal Orhan, Mehmet Tuzcu, Kazim Sahin, Ibrahim Hanifi Ozercan, Ibrahim Halil Bahçecioğlu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

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  13. Review
  14. Effect of amlodipine, lisinopril and allopurinol on acetaminophen-induced hepatotoxicity in rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2016
    Article
  15. Article
  16. Article
  17. The Role of Oxidative Stress and Antioxidants in Liver Diseases.International journal of molecular sciences · 2015
    Review
  18. Article
  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

8 authors at 1 institution in 1 country.

Ulvi DemirelDepartment of Gastroenterology, School of Medicine, Firat University, 23119, Elazig, Turkey. drudemirel@hotmail.com
Mehmet Yalniz
Cem Aygün
Cemal Orhan
Mehmet Tuzcu
Kazim Sahin
Ibrahim Hanifi Ozercan
Ibrahim Halil Bahçecioğlu
Fırat University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays important role in the development of acute liver failure. In this study, we investigated effects of allopurinol (AP) upon thioacetamide (TAA)-induced liver injury and the potential mechanisms leading to amelioration in inflammation with AP treatment. Acute liver failure was induced by intraperitoneal administration of TAA (300 mg/kg/day for 2 days). Thirty-five rats were divided into five groups as control (group 1), TAA (group 2), TAA + 25AP (group 3), TAA + 50 AP (group 4), and TAA + 100AP (group 5). The number of animals in each group was seven. At the end of the study, histopathological, biochemical, and western blot analysis were done. TAA treatment significantly increased serum levels of aminotransferases, liver malondialdehyde (MDA), nuclear factor-kappa B (NF-қB ), activator protein-1 (AP-1), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2) and interleukin-6 (IL-6) levels, and the necro-inflammation scores. Nevertheless, nuclear factor E2-related factor-2 and heme oxygenase-1 (HO-1) expressions in the liver were decreased by TAA. AP treatment significantly lowered the serum levels of aminotransferases (P < 0.01) and liver MDA, NF-κB, AP-1, TNF-α, COX-2, and IL-6 expressions (P < 0.05). Moreover, AP restored the liver Nrf2 and HO-1 expressions and improved the necro-inflammation scores significantly. AP improves oxidative stress-induced liver damage by regulating cellular redox-sensitive transcriptor factors and expression of pro-inflammatory and antioxidant defense mechanisms. AP probably exerts these beneficiary features by its free radical scavenging ability in a dose-dependent manner.

Indexed as

AllopurinolAnimalsAntioxidantsChemical and Drug Induced Liver InjuryCyclooxygenase 2Heme Oxygenase-1InflammationInterleukin-6Liver Failure, AcuteMaleMalondialdehydeNF-E2-Related Factor 2NF-kappa BOxidation-ReductionOxidative StressRatsAllopurinolAntioxidantsCyclooxygenase 2Heme Oxygenase-1Interleukin-6MalondialdehydeNF-E2-Related Factor 2NF-kappa BReactive Oxygen SpeciesThioacetamideTransaminasesTranscription Factor AP-1Transcription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID22535497
OpenAlexW2010561802

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.