Glycyrrhizin Improves Fatty Liver Symptoms, Increases Adiponectin and Reduces UCP2 Expression in Wistar Rats

被引:3
作者
Bagheri H. [1 ]
Yaghmaei P. [1 ]
Modaresi M. [2 ]
Sabbaghian M. [3 ]
Ebrahim-Habibi A. [4 ,5 ]
机构
[1] Department of Biology, Science and Research Branch, Islamic Azad University, Tehran
[2] Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran
[3] Department of Andrology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran
[4] Biosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Jalal-al-Ahmad Street, Chamran Highway, Tehran
[5] Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran
关键词
Cholesterol; Glycyrrhizin; NAFLD; UCP2;
D O I
10.1007/s40011-019-01097-7
中图分类号
学科分类号
摘要
Glycyrrhizin (GL) is the main bioactive component in the extract of licorice root, with beneficial effects on metabolic syndrome. This study investigates the effect of GL on biochemical and histological parameters and UCP2 gene expression in a rodent nonalcoholic steatosis model. Thirty-two male Wistar rats were classified into four groups randomly: control (normal diet with standard rat chow), high-cholesterol diet (HCD for 12 weeks) and two experimental groups (HCD for 12 weeks then shifted to normal diet plus receiving either 20 mg/kg or 100 mg/kg of glycyrrhizin for 4 weeks). At the end of experiment, in the HCD group, body weight, glucose and insulin levels were increased, lipid profile was impaired, and the markers related to liver were abnormal, while adiponectin, catalase and superoxide dismutase levels were decreased. Histological analysis of liver sections showed the appearance of hepatic fibrosis and steatosis, and UCP2 gene expression was increased significantly. GL treatment at both doses and especially at 100 mg/kg ameliorated the situation, and levels of UCP2 were decreased significantly. In conclusion, administration of glycyrrhizin can improve liver fibrosis through down-regulating the UCP2 expression. © 2019, The National Academy of Sciences, India.
引用
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页码:191 / 197
页数:6
相关论文
共 27 条
[1]  
Kotronen A., Yki-Jarvinen H., Fatty liver, Arterioscler Thromb Vasc Biol, 28, 1, pp. 27-38, (2008)
[2]  
Oosterveer M.H., Van Dijk T.H., Tietge U.J., Boer T., Havinga R., Stellaard F., Groen A.K., Kuipers F., Reijngoud D.-J., High fat feeding induces hepatic fatty acid elongation in mice, PLoS ONE, 4, 6, (2009)
[3]  
Hubscher S., Histological assessment of non-alcoholic fatty liver disease, Histopathology, 49, 5, pp. 450-465, (2006)
[4]  
Wu X., Zhang L., Gurley E., Studer E., Shang J., Wang T., Wang C., Yan M., Jiang Z., Hylemon P.B., Prevention of free fatty acid–induced hepatic lipotoxicity by 18β-glycyrrhetinic acid through lysosomal and mitochondrial pathways, Hepatology, 47, 6, pp. 1905-1915, (2008)
[5]  
Sacco R., Pucci L., Sivozhelezov V., Pellegrini L., Giacomelli L., Longo V., Prevention of vascular damage with Lisosan G wheat extract: the in vitro basis for a clinical investigation, Eur Rev Med Pharmacol Sci, 19, 8, pp. 1517-1519, (2015)
[6]  
Fernando H.A., Chandramouli C., Rosli D., Lam Y.L., Yong S.T., Yaw H.P., Ton S.H., Kadir K.A., Sainsbury A., Glycyrrhizic acid can attenuate metabolic deviations caused by a high-sucrose diet without causing water retention in male Sprague-Dawley rats, Nutrients, 6, 11, pp. 4856-4871, (2014)
[7]  
El-Magd N.F.A., El-Karef A., El-Shishtawy M.M., Eissa L.A., Hepatoprotective effects of glycyrrhizin and omega-3 fatty acids on Nuclear Factor-kappa B pathway in thioacetamide-induced fibrosis in rats, Egypt J Basic Appl Sci, 2, 2, pp. 65-74, (2015)
[8]  
Pecqueur C., Alves-Guerra M.-C., Gelly C., Levi-Meyrueis C., Couplan E., Collins S., Ricquier D., Bouillaud F., Miroux B., Uncoupling protein 2, in vivo distribution, induction upon oxidative stress, and evidence for translational regulation, J Biol Chem, 276, 12, pp. 8705-8712, (2001)
[9]  
Echtay K.S., Murphy M.P., Smith R.A., Talbot D.A., Brand M.D., Superoxide activates mitochondrial uncoupling protein 2 from the matrix side Studies using targeted antioxidants, J Biol Chem, 277, 49, pp. 47129-47135, (2002)
[10]  
Brand M.D., Esteves T.C., Physiological functions of the mitochondrial uncoupling proteins UCP2 and UCP3, Cell Metab, 2, 2, pp. 85-93, (2005)