Evidence map›Paper›PMID 28966758›Full record

ArticleInternational journal of preventive medicine2017

Effect of Angiotensin-converting Enzyme Inhibitor on Cardiac Fibrosis and Oxidative Stress Status in Lipopolysaccharide-induced Inflammation Model in Rats.

Azam Abareshi, Fatemeh Norouzi, Fereshteh Asgharzadeh, Farimah Beheshti, Mahmoud Hosseini, Mehdi Farzadnia, Majid Khazaei

Open access · goldAbstract read
In one paragraph

Article in International journal of preventive medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 39 citations in OpenAlex.

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  14. Cardiac fibrosis: potential therapeutic targets.Translational research : the journal of laboratory and clinical medicine · 2019
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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.

Azam AbareshiDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Fatemeh NorouziDepartment of Physiology, School of Medicine, Esfarayen Faculty of Medical Sciences, Esfarayen, Iran.
Fereshteh AsgharzadehDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Farimah BeheshtiDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mahmoud HosseiniNeurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mehdi FarzadniaDepartment of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Majid KhazaeiNeurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenin-angiotensin (Ang)-aldosterone system not only plays a key role in the regulation of circulatory homeostasis, but also it acts as a powerful pro-inflammatory mediator. The aim of this study was to evaluate the effect of captopril (Cap), a known Ang-converting enzyme inhibitor, on inflammation-induced cardiac fibrosis, and heart oxidative stress status in lipopolysaccharide (LPS)-induced inflammation in male rats.

methodsFifty male rats were randomly divided into five groups control, LPS (1 mg/kg/day), LPS + Cap 10 mg/kg, LPS + Cap 50 mg/kg and LPS + Cap 100 mg/kg. After 2 weeks, blood samples were taken, and hearts were harvested for evaluation of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide metabolite in serum and tissue hemogenate, histopathology (hematoxylin and eosin and Masson's trichrome) and oxidative stress status.

resultsSerum IL-6 and TNF-α concentration were higher in LPS group compared to control and Cap reduced them, significantly. Heart TNF-α and IL-6 contents in LPS group were significantly higher than control (

conclusionsTreatment by Cap reduced cardiac fibrosis possibly through improving oxidative stress status, and it can be considered to increase cardiac compliance in this condition.

Indexed as

Angiotensincardiacfibrosisinflammation

Identifiers

PMID28966758
PMCPMC5609356
OpenAlexW2750996608

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.