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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，一种类蛋白受体1拮抗剂，在大鼠模型中的非酒精性脂肪肝病通过调节Activin A和Follistatin的肝脏表达

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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（NAFLD）是肝脏发病率和死亡率的主要原因，目前还没有有效的治疗方法。内源性大麻素系统在各种肝脏疾病中起着重要作用。激活素A是转化生长因子β（TGF-β）超家族的成员，可抑制肝细胞生长。富利他汀拮抗激活素A的生物学作用。本研究旨在研究利莫那班（一种有效的大麻素受体1（CB1）拮抗剂）对胆碱缺乏（CD）饮食诱导的大鼠NAFLD的影响，并检测其是否能改变激活素A和富利他汀的肝脏表达。40只大鼠分为4组：对照组、利莫那班治疗组（接受利莫那班治疗的正常大鼠）；镉饮食组（镉饮食诱导的NAFLD）；CD饮食+利莫那班组（利莫那班治疗NAFLD）。结果发现，CD饮食导致肝指数、血清肝酶水平、肝组织中丙二醛（MDA）、TGF-β1、激活素A和CB1表达显著增加，肝组织中谷胱甘肽过氧化物酶（GSH-Px）和卵泡抑素mRNA表达显著降低。与单独喂食CD组相比，服用利莫那班显著改善了所有研究参数。组织病理学检查支持这些结果。我们得出结论，利莫那班通过降低氧化应激和肝脏TGF-β1的表达，并调节肝脏激活素A和卵泡抑素的表达，显著对抗CD饮食诱导的NAFLD。

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