• Min Suk Seo, Sung-Woon Hong, Sung Hum Yeon, Young-Mok Kim, Key An Um, Jung Hwan Kim, Hye Jung Kim, Ki Churl Chang, and Sang Won Park.
• Department of Pharmacology, School of Medicine, Institute of Health Sciences, Gyeongsang National University, 816-15 Jinjudaero, Jinju 660-751, Republic of Korea.
• J Ethnopharmacol. 2014 Nov 18; 157: 140-8.

Ethnopharmacological RelevanceMagnolia officinalis (MO) is a traditional Chinese herbal medicine that has been used in clinical practice to treat liver disease. The aim of this study is to examine the effects of MO on the development of nonalcoholic fatty liver in hepatocytes.Materials And MethodsHuman hepatoma-derived HepG2 cells and mouse normal FL83B hepatocytes were exposed to 0.5mM free fatty acids (FFAs; oleate:palmitate, 2:1) for 24h to simulate conditions of nonalcoholic fatty liver in vitro. The cells were treated with a standardized MO extract 1h prior to FFA exposure.ResultsMO pretreatment attenuated the increases in intracellular lipid accumulation and triglyceride content in FFA-exposed hepatocytes in a dose-dependent manner. MO pretreatment significantly inhibited both sterol regulatory element-binding protein (SREBP)-1c activation and increases in fatty acid translocase, fatty acid synthase, and stearoyl CoA desaturase-1 protein expression in FFA-exposed hepatocytes in a dose-dependent manner. MO pretreatment markedly induced adenosine monophosphate-activated protein kinase (AMPK) phosphorylation in hepatocytes. Compound C, an AMPK inhibitor, blocked the inhibitory effect of MO on the increases in intracellular lipid accumulation and triglyceride content induced by FFAs. In hepatocytes pretreated with compound C, MO failed to inhibit SREBP-1c activation and the increases in fatty acid translocase, fatty acid synthase, and stearoyl-CoA desaturase-1 protein expression induced by FFAs.ConclusionsOur results indicate that MO attenuates triglyceride biosynthesis and accumulation induced by FFAs in hepatocytes, suggesting its pharmacological potential for the prevention of nonalcoholic fatty liver disease. These effects may be mediated by the inhibition of SREBP-1c via AMPK phosphorylation.Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

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