混合源性脂肪肝的生物模型

T. V. Brus, Andrei G. Vasiliev, Aleftina A. Kravcova, Anna V. Vasilieva, Yurii S. Brus, Anastasia V. Bannova
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摘要

背景:代谢性和中毒性肝病主要包括非酒精性脂肪肝、酒精性脂肪肝和混合性脂肪变性。目前,由于对非感染性肝病的病因和发病机理缺乏明确的认识,还没有预防和治疗这些病症的有效方法。研究病因和发病机制的关键在于寻找适当的肝衰竭实验模型。目的:建立、测试和评估混合型脂肪肝的实验模型。材料与方法:研究对象为 30 只雄性白化灰白 Wistar 大鼠。实验组大鼠在加入实验时体重为 180-200 克,连续 30 天每天摄入 20 克颗粒状啮齿动物食物,其中添加 6 克结晶果糖(占总食物的 30%),并在饮水碗中加入 10%的乙醇溶液代替饮用。结果:在实验组中,天门冬氨酸氨基转移酶、丙氨酸氨基转移酶和碱性磷酸酶的水平出现了统计学意义上的显著上升,这证实了细胞溶解和胆汁淤积综合征的发生。尸检肝脏标本显示肝细胞脂肪变性的组织学图像。结论:为了实现这一目标,我们开发了一种方法来模拟混合型脂肪肝。高碳水化合物和富含乙醇的饮食导致肝脏病理过程迅速发展。该研究表明,结合病史、细胞溶解和胆汁淤积综合征的实验室指标,对肝脏进行详细的形态学研究,以鉴别诊断各种病因引起的脂肪肝是可行的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Biomodeling of mixed origin fatty liver disease
BACKGROUND: The main examples of liver pathology of metabolic and toxic origin are non-alcoholic, alcoholic fatty liver disease and fatty degeneration of mixed origin. Currently, due to the lack of a clear understanding of the causes and pathogenesis of hepatopathy of non-infectious origin, there are no effective methods for the prevention and treatment of these conditions. A key role in studying the etiology and mechanisms of pathogenesis is played by the search for adequate experimental models of liver failure. AIM: To develop, test and evaluate an experimental model of mixed fatty liver disease. MATERIALS AND METHODS: The study was conducted on 30 male albino gray Wistar rats. Experimental rats, weighing 180–200 grams at the time of inclusion in the experiment, received granulated rodent food weighing 20 grams daily for 30 days, to which 6 g of crystalline fructose was introduced (at the rate of 30% of the total diet), and instead of drinking 10% ethyl alcohol solution was given freely available in the drinking bowl. RESULTS: In experimental group, there was a statistically significant increase in the level of aspartate aminotransferase, alanylaminotransferase, and alkaline phosphatase, which confirms the development of cytolytic and cholestatic syndromes. Autopsy liver specimens showed a histological picture of fatty degeneration of hepatocytes. CONCLUSIONS: To achieve this goal, a method was developed for modeling fatty liver of mixed origin. A high-carbohydrate and ethanol-rich diet led to the rapid development of pathological processes in the liver. The study demonstrated the feasibility of a detailed morphological study of the liver, taking into account medical history, laboratory indicators of cytolytic and cholestatic syndromes for the differential diagnosis of fatty liver of various etiologies.
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