A modified high-fat diet and its effect on histopathological features of mice liver as an alternative diet for animal model of liver cell damage

Dzul Fithria Mumtazah, H. Busman, M. Kanedi, G. Pratami
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Abstract

Researchers attempted to obtain animal models that experienced hypercholesterolemia and led to liver damage to determine the performance of the liver. Rats were chosen because of the ease of handling, collecting organ and blood samples. Still, their high price and availability that are more difficult to find have made some researchers look for alternatives to other animal models such as mice. This study aims to determine the role of a modified high-fat diet as an alternative diet for mice to experience hepar damage. Male mice treated for four and eight weeks with a modified high-fat diet were sacrificed for their liver, then they were tested for histopathology using the paraffin method and HE staining. The characterization of hepar damage traits was carried out to score the degree of parenchymal degeneration, hydropic degeneration, and necrosis. The results showed that the control group, four and eight weeks of atherogenic diet had more than 50% cell damage, presumably due to the role of the starch mixture in feed as a source of carbohydrates through the mechanism of converting carbohydrate pathways into fat which damages liver cells.
改良高脂饮食对肝细胞损伤动物模型小鼠肝脏组织病理学的影响
研究人员试图获得经历高胆固醇血症并导致肝损伤的动物模型,以确定肝脏的性能。选择大鼠是因为易于处理,收集器官和血液样本。尽管如此,它们的高价格和更难以找到的可用性使得一些研究人员寻找其他动物模型(如小鼠)的替代品。本研究旨在确定改良高脂肪饮食作为小鼠肝损伤的替代饮食的作用。用改良高脂饮食治疗4周和8周的雄性小鼠,取肝脏,石蜡法和HE染色进行组织病理学检查。对肝实质变性、积水变性和坏死程度进行肝损伤特征表征。结果显示,对照组,4周和8周的致动脉粥样硬化饮食有超过50%的细胞损伤,可能是由于饲料中的淀粉混合物作为碳水化合物的来源,通过将碳水化合物途径转化为脂肪的机制,损害肝细胞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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