1. Magnolia officinalis attenuates free fatty acid-induced lipogenesis via AMPK phosphorylation in hepatocytes.
- Author
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Seo, Min Suk, Hong, Sung-Woon, Yeon, Sung Hum, Kim, Young-Mok, Um, Key An, Kim, Jung Hwan, Kim, Hye Jung, Chang, Ki Churl, and Park, Sang Won
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LIPID metabolism , *FATTY liver prevention , *ENZYME metabolism , *ADENOSINE monophosphate , *ALTERNATIVE medicine , *ANIMAL experimentation , *BIOLOGICAL models , *CARRIER proteins , *DOSE-response relationship in biochemistry , *BOTANIC medicine , *CHINESE medicine , *MICE , *PHOSPHORYLATION , *PROTEIN kinases , *TRIGLYCERIDES , *PLANT extracts , *STATISTICAL significance , *DESCRIPTIVE statistics , *IN vitro studies - Abstract
Ethnopharmacological relevance Magnolia 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 methods Human hepatoma-derived HepG2 cells and mouse normal FL83B hepatocytes were exposed to 0.5 mM free fatty acids (FFAs; oleate:palmitate, 2:1) for 24 h to simulate conditions of nonalcoholic fatty liver in vitro . The cells were treated with a standardized MO extract 1 h prior to FFA exposure. Results MO 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. Conclusions Our 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. [ABSTRACT FROM AUTHOR] more...
- Published
- 2014
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