实验化学性与酒精性肝纤维化大鼠动物模型的比较

目的:比较实验化学性与酒精性肝纤维化大鼠动物模型的病理改变的不同.方法:选取Wistar纯系大白鼠皮下多点反复注射四氯化碳复制化学性肝纤维化动物模型.通过递增乙醇浓度,日3次胃内灌注乙醇来复制酒精性肝纤维化动物模型.分别于第4周,第8周,第12周末进行肝脏重量,肝脏病理学以及电镜下贮脂细胞的检测.结果:化学性肝纤维化组,4周末肝脏呈点状坏死,贮脂细胞开始活化;8周末肝脏呈大片状坏死,贮脂细胞活化明显;12周末,形成较完整的纤维间隔,贮脂细胞成为肌成纤维样细胞,并分泌大量胶原.酒精性肝纤维化组,4周末肝细胞中度脂肪变性,贮脂细胞无明显活化;8周末肝细胞变性坏死,贮脂细胞开始活化;12周末,形成轻度纤维化改变,贮脂细胞活化明显并分泌大量胶原.结论:化学性及酒精性肝纤维化发展过程存在不同的发病机制.

Comparison of experimental chemical and alcoholic liver fibrosis animal model

Objective: To compare the difference of pathology in animal models of chemical and alcoholic liver fibrosis.Methods:Male Wistar rats were used . The chemical liver fibrosis was induced by polypoint subcutaneous injection of carbon tetrachloride.The rat model of alcoholic liver fibrosis was induced by intragastric infusion of increasing concentration of ethanol 3 times per day. The animals were killed 4,8,12 weeks late separately. The weight of liver, pathology of liver, and morphology of fat storing cell(FSC) were examined. Results:In the chemical liver fibrosis group , at the end of the 4th week, pathology showed point necrosis, and FSC began to be activated. At the end of the 8th week , pathology showed large area of necrosis, and FSC was activated obviously. At the end of the 12th week, relative integrated septum was formed, and FSC changed into myofibroblast and secreted collagen. In the alcoholic liver fibrosis group, at the end of the 4th week, pathology showed moderate to severe steatosis, and FSC was not activated. At the end of the 8th week, hepatocyte necrosis and inflammation were found, and FSC began to be activated. At the end of the 12th week, mild fibrosis was found, FSC was activated and secreted collagen. Conclusion: The chemical and alcohol liver fibrosis may exist different mechanisms in pathogenesis.