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
Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroenterol Hepatol Bed Bench. 2017 Winter;10(Suppl1):S122-S128.
This study is presenting an effective method of inducing liver fibrosis by CCL4 as a toxin in two different breeds of rat models.
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.
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.
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.
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.
本研究提出了一种在两种不同品系大鼠模型中用四氯化碳作为毒素诱导肝纤维化的有效方法。
肝纤维化是伤口愈合反应引起的炎症和肝损伤的结果，最终导致肝衰竭。因此，肝纤维化后，病情会继续发展为肝硬化，最终发展为肝细胞癌（HCC）。许多研究表明，肝纤维化最重要的原因之一是非酒精性脂肪性肝炎（NASH）。纤维化肝脏受到胶原蛋白和α-SMA等细胞外基质（ECM）蛋白过度积累的影响。
在两个不同的实验中，使用体重200±60克、年龄约10周的雄性维斯塔大鼠和斯普拉格-道利大鼠模型来诱导四氯化碳处理的肝纤维化。
在注射四氯化碳6周后，进行了不同的测试以验证肝纤维化，包括血清标志物如天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）、分子测试包括层粘连蛋白和α-SMA，以及在纤维化组和对照组中通过苏木精和伊红染色进行病理观察。
病理学和实时PCR结果表明，与维斯塔大鼠相比，斯普拉格-道利大鼠模型中肝纤维化的诱导效果更好。
