Effects of (−)-epicatechin on the time course of the expression of perilipins in a diet-induced model of nonalcoholic steatohepatitis

非酒精性脂肪性肝炎 内科学 课程(导航) 脂肪性肝炎 表达式(计算机科学) 化学 非酒精性脂肪肝 脂肪肝 计算机科学 工程类 医学 航空航天工程 程序设计语言 疾病
作者
Isabel Hidalgo,Nayelli Nájera,Eduardo Meaney,Javier Pérez‐Durán,María Yolotzin Valdespino-Vázquez,Francisco Villarreal,Guillermo Ceballos
出处
期刊:Journal of Nutritional Biochemistry [Elsevier BV]
卷期号:77: 108296-108296 被引量:14
标识
DOI:10.1016/j.jnutbio.2019.108296
摘要

The existing treatments for nonalcoholic steatohepatitis (NASH) are not completely effective. The need for new alternatives without adverse effects and low cost, such as the flavonoid (−)-epicatechin (EC), which has beneficial effects on lipid metabolism and cardiovascular diseases, arises. The objective of this work was to analyze EC effects in the NASH induced by a Paigen-type diet (PD). Mice were administered with (1) normal chow and water, (2) PD + fructose 30% and (3) PD + fructose 30% + EC (1 mg/kg) per gavage during 9 weeks. At the end of each treatment, serum was collected for analysis of the biochemical profile and liver enzymes. The liver was collected for microscopic analysis and for the evaluation of the relative expression of Plin2, Plin3, CD36, adiponectin and UCP2. Results showed that EC reduced weight gain and decreased triglyceride (TG), low-density lipoprotein cholesterol, TG/high-density lipoprotein and the activity of liver enzymes (alanine aminotransferase and alkaline phosphatase), suggesting lower liver damage. The microscopic analysis showed less “balloonization” of the hepatocyte, small drops of lipids, less accumulation of collagen and infiltration of inflammatory cells as compared to nontreated group. Finally, a decrease in the expression of Plin 2 was observed. While CD36 decreased, adiponectin and UCP2 increased. In conclusion, EC improves the biochemical profile, the microscopic characteristics and protein expression. Therefore, it may be a possible therapeutic approach for NASH since it prevents the progression of the hepatic and metabolic damage induced by high-fat diets.

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