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Meysam Nasiri

Assistanr Professor of Cell and Molecular Biology

Education

  • Ph.D. 2011-2017

    Cellular & Molecular Biology

    Shiraz University, Shiraz, Iran

  • M.Sc. 2008-2010

    Electronic Engineering

    Shiraz University, Shiraz, Iran

Selected Publications

Gitiara, A., Tokhanbigli, S., Mazhari, S., Baghaei, K., Hatami, B., Hashemi, S.M., Rad, A.A., Moradi, A., Nasiri, M., Ahrabi, N.Z., Zali, M.R. Development of experimental fibrotic liver diseases animal model by Carbon Tetracholoride (2017) Gastroenterology and Hepatology from Bed to Bench, 10, pp. S122-S128.

DOI: 10.22037/ghfbb.v0i0.1269

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. © 2017 RIGLD, Research Institute for Gastroenterology and Liver Diseases.

AUTHOR KEYWORDS: Animal model; CCL4; Liver fibrosis
INDEX KEYWORDS: alanine aminotransferase; alpha smooth muscle actin; aspartate aminotransferase; carbon tetrachloride; collagen type 4; laminin; olive oil; scleroprotein, alanine aminotransferase blood level; aminotransferase blood level; animal cell; animal experiment; animal model; animal tissue; Article; bioaccumulation; biochemical analysis; body weight; carbon tetrachloride-induced liver fibrosis; cell enlargement; comparative study; controlled study; degradation; disease course; disease exacerbation; disease severity; extracellular matrix; genetic analysis; hepatic stellate cell; histochemistry; histopathology; in vivo study; lipid liver level; liver function; male; nonalcoholic fatty liver; nonhuman; protein expression; quantitative analysis; rat; real time polymerase chain reaction; Sprague Dawley rat; Wistar rat
PUBLISHER: Research Institute for Gastroenterology and Liver Diseases

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