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Cited 32 time in webofscience Cited 34 time in scopus
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Magnolia officinalis attenuates free fatty acid-induced lipogenesis via AMPK phosphorylation in hepatocytes

Authors
Seo, Min SukHong, Sung-WoonYeon, Sung HumKim, Young-MokUm, Key AnKim, Jung HwanKim, Hye JungChang, Ki ChurlPark, Sang Won
Issue Date
18-Nov-2014
Publisher
ELSEVIER IRELAND LTD
Keywords
AMP-activated protein kinase; Magnolia officinalis; Nonalcoholic fatty liver; Sterol regulatory element-binding protein-1c
Citation
JOURNAL OF ETHNOPHARMACOLOGY, v.157, pp 140 - 148
Pages
9
Indexed
SCI
SCIE
SCOPUS
Journal Title
JOURNAL OF ETHNOPHARMACOLOGY
Volume
157
Start Page
140
End Page
148
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/18654
DOI
10.1016/j.jep.2014.09.031
ISSN
0378-8741
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. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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