Triterpenic acids-enriched fraction from Cyclocarya paliurus attenuates non-alcoholic fatty liver disease via improving oxidative stress and mitochondrial dysfunction

• Published in: Biomedicine & pharmacotherapy Vol. 104; pp. 229 - 239
• Main Authors: Zhao, Meng-ge, Sheng, Xue-ping, Huang, Ya-ping, Wang, Yi-ting, Jiang, Cui-hua, Zhang, Jian, Yin, Zhi-qi
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.08.2018
• Subjects: Cyclocarya paliurus triterpenic acids; Mitochondrial dysfunction; Nonalcoholic fatty liver disease; Oxidative stress; Oxidative stress; Cyclocarya paliurus triterpenic acids; Nonalcoholic fatty liver disease; Mitochondrial dysfunction
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.03.170

The effects of triterpenic acids-enriched fraction from Cyclocarya paliurus (CPT) on nonalcoholic fatty liver disease (NAFLD) were investigated using in vivo and in vitro models. In high fat diet-induced Wister rats, CPT significantly increased superoxide dismutase (SOD) activity and glutathione/oxidized glutathione (GSH/GSSG) ratio, reduced malondialdehyde (MDA) and protein carbonyl (PCO) levels. Moreover, CPT restored mitochondrial membrane potential dysfunction, decreased cytochrome P450 enzyme 2E1 (CYP2E1) activity, improved nuclear factor erythroid 2-related factor 2 (Nrf2) and Nrf2-mediated antioxidant enzyme heme oxygenase1 (HO-1) expression. In free fatty acids-induced HepG2 cells, CPT dramatically decreased ROS content, increased mitochondrial NADH dehydrogenase (Complex I) and mitochondrial cytochrome C oxidase (Complex IV) levels. Furthermore, CPT could upregulate HO-1, quinine oxidoreductase 1 (NQO1) expression, and increase Nrf2 translocation from cytoplasm-to-nucleus. The results indicated CPT could protect mitochondria function and improve oxidative stress by activating Nrf2. Therefore, it can be inferred that CPT may be a potential agent against NAFLD.