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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Protective effect of rimonabant, a canabinoid receptor 1 antagonist, on nonalcoholic fatty liver disease in a rat model through modulation of the hepatic expression of activin A and follistatin
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Protective effect of rimonabant, a canabinoid receptor 1 antagonist, on nonalcoholic fatty liver disease in a rat model through modulation of the hepatic expression of activin A and follistatin

机译：rimonabant，一种大麻素受体1拮抗剂，通过调节Activin A和follistatin的肝化性表达的大鼠模型中非酒精性脂肪肝病的保护作用

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Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver morbidity and mortality, and there is still no proven effective therapy. The endocannabinoid system plays an important role in various liver diseases. Activin A is a member of the transforming growth factor beta (TGF-β) superfamily and inhibits hepatocyte growth. Follistatin antagonizes the biological actions of activin A. This study was designed to investigate the effect of rimonabant (a potent cannabinoid receptor1 (CB1) antagonist) on NAFLD induced with a choline-deficient (CD) diet in rats, as well as to detect whether it can alter the hepatic expression of activin A and follistatin. Forty rats were distributed among 4 groups: the control group, the rimonabant treatment group (normal rats that received rimonabant); the CD diet group (NAFLD induced with a CD diet); and the CD diet + rimonabant group (NAFLD treated with rimonabant). It was found that the CD diet caused significant increase in liver index, serum levels of liver enzymes, malondialdehyde (MDA), TGF-β1, activin A, and CB1 expression in liver tissue, with a significant decrease in glutathione peroxidase (GSH-Px) and follistatin mRNA expression in liver tissues. The administration of rimonabant significantly improved all of the studied parameters compared with the group fed the CD diet alone. Histopathological examination supported these results. We concluded that rimonabant significantly counteracted NAFLD induced with the CD diet by decreasing oxidative stress and hepatic expression of TGF-β1, and modulating the hepatic expression of activin A and follistatin.
机译：非酒精性脂肪肝病（NAFLD）是肝脏发病率和死亡率的主要原因，仍然没有经过遗传的有效治疗。 Endocannabinoid系统在各种肝病中起重要作用。 Actiacin A是转化生长因子β（TGF-β）超家族的成员，并抑制肝细胞生长。 Follistatin拮抗Activin A的生物学作用。该研究旨在探讨rimonabant（有效的大麻素受体1（CB1）拮抗剂）对大鼠胆碱缺陷（CD）饮食诱导的NAFLD的影响，以及检测是否它可以改变Actiacin A和Follistatin的肝脏表达。四十只大鼠分布在4组中：对照组，缩编治疗组（接受缩轮夹的正常大鼠）; CD饮食组（NAFLD诱导CD饮食）;和CD饮食+ rimonabant组（Nafld用rimonabant治疗）。发现CD饮食导致肝脏指数，肝脏血清水平，丙氨醛（MDA），TGF-β1，激活素A和CB1表达的显着增加，谷胱甘肽过氧化物酶的显着降低（GSH-PX ）和肝组织中的Follistatin mRNA表达。与喂养CD饮食单独的组相比，乙月蛋白的给药显着改善了所有研究的参数。组织病理学检查支持这些结果。我们得出结论，通过降低TGF-β1的氧化应激和肝脏表达，通过降低氧化胁迫和肝脏表达，调节活性蛋白A和Follistatin的肝脏表达，乙月植物显着抵消了CD饮食的NAFLD。

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