Evidence map›Paper›PMID 29511482›Full record

ArticleGastroenterology and hepatology from bed to bench2017

Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride.

Atoosa Gitiara, Samaneh Tokhanbigli, Sogol Mazhari, Kaveh Baghaei, Behzad Hatami, Seyed Mahmoud Hashemi, Ali Asadi Rad, Afshin Moradi, Meyam Nasiri, Nakisa Zarrabi Ahrabi and 1 more

Abstract read
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Article in Gastroenterology and hepatology from bed to bench, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. 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

11 authors.

Atoosa GitiaraBasic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Samaneh TokhanbigliBasic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Sogol MazhariBasic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Kaveh BaghaeiGastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Behzad HatamiGastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Seyed Mahmoud HashemiDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Ali Asadi RadDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Afshin MoradiGastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Meyam NasiriDepartment of Biology, Damghan University, Damghan, Iran.
Nakisa Zarrabi AhrabiDepartment of Biology Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Mohammad Reza ZaliGastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThis study is presenting an effective method of inducing liver fibrosis by CCL4 as a toxin in two different breeds of rat models.

backgroundLiver fibrosis is a result of inflammation and liver injury caused by wound healing responses which ultimately lead to liver failure. Consequently, after liver fibrosis, the progression will be continued to liver cirrhosis and at the end stage hepatocellular carcinoma (HCC). Many studies have demonstrated that one of the most important causes of liver fibrosis is Non-alcoholic steatohepatitis (NASH). Fibrotic Liver is affected by an excessive accumulation of extracellular matrix (ECM) proteins like collagen and α-SMA.

methodsIn two different experiments, male Vistar, and Sprague Dawley Rat models ranging from 200±60, corresponding to an age of approximately 10 weeks were utilized in order to induce CCL4 treated liver fibrosis.

resultsAfter 6 weeks of CCL4 injection, different tests have been carried out to verify the liver fibrosis including serum markers such as Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT), molecular tests containing, laminin and α-SMA and also pathological observation by Hematoxylin and eosin staining in both fibrosis and control group.

conclusionThe results of Pathology and Real-time PCR showed that fibrosis was induced much more effectively in Sprague Dawley rat model compared with Wistar rats.

Indexed as

Animal ModelCCL4Liver Fibrosis

Identifiers

PMID29511482
PMCPMC5838191

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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.