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Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride
AIM: This study is presenting an effective method of inducing liver fibrosis by CCL4 as a toxin in two different breeds of rat models. BACKGROUND: Liver fibrosis is a result of inflammation and liver injury caused by wound healing responses which ultimately lead to liver failure. Consequently, after...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Shaheed Beheshti University of Medical Sciences
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5838191/ https://www.ncbi.nlm.nih.gov/pubmed/29511482 |
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author | Gitiara, Atoosa Tokhanbigli, Samaneh Mazhari, Sogol Baghaei, Kaveh Hatami, Behzad Hashemi, Seyed Mahmoud Asadi Rad, Ali Moradi, Afshin Nasiri, Meyam Zarrabi Ahrabi, Nakisa Zali, Mohammad Reza |
author_facet | Gitiara, Atoosa Tokhanbigli, Samaneh Mazhari, Sogol Baghaei, Kaveh Hatami, Behzad Hashemi, Seyed Mahmoud Asadi Rad, Ali Moradi, Afshin Nasiri, Meyam Zarrabi Ahrabi, Nakisa Zali, Mohammad Reza |
author_sort | Gitiara, Atoosa |
collection | PubMed |
description | AIM: This study is presenting an effective method of inducing liver fibrosis by CCL4 as a toxin in two different breeds of rat models. BACKGROUND: Liver 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. METHODS: In 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. RESULTS: After 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. CONCLUSION: The results of Pathology and Real-time PCR showed that fibrosis was induced much more effectively in Sprague Dawley rat model compared with Wistar rats. |
format | Online Article Text |
id | pubmed-5838191 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Shaheed Beheshti University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-58381912018-03-06 Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride Gitiara, Atoosa Tokhanbigli, Samaneh Mazhari, Sogol Baghaei, Kaveh Hatami, Behzad Hashemi, Seyed Mahmoud Asadi Rad, Ali Moradi, Afshin Nasiri, Meyam Zarrabi Ahrabi, Nakisa Zali, Mohammad Reza Gastroenterol Hepatol Bed Bench Original Article AIM: This study is presenting an effective method of inducing liver fibrosis by CCL4 as a toxin in two different breeds of rat models. BACKGROUND: Liver 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. METHODS: In 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. RESULTS: After 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. CONCLUSION: The results of Pathology and Real-time PCR showed that fibrosis was induced much more effectively in Sprague Dawley rat model compared with Wistar rats. Shaheed Beheshti University of Medical Sciences 2017 /pmc/articles/PMC5838191/ /pubmed/29511482 Text en ©2017 RIGLD, Research Institute for Gastroenterology and Liver Diseases This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Gitiara, Atoosa Tokhanbigli, Samaneh Mazhari, Sogol Baghaei, Kaveh Hatami, Behzad Hashemi, Seyed Mahmoud Asadi Rad, Ali Moradi, Afshin Nasiri, Meyam Zarrabi Ahrabi, Nakisa Zali, Mohammad Reza Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title | Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title_full | Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title_fullStr | Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title_full_unstemmed | Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title_short | Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride |
title_sort | development of experimental fibrotic liver diseases animal model by carbon tetracholoride |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5838191/ https://www.ncbi.nlm.nih.gov/pubmed/29511482 |
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