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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 3140267, 11 pages
Research Article

Zanthoxylum ailanthoides Suppresses Oleic Acid-Induced Lipid Accumulation through an Activation of LKB1/AMPK Pathway in HepG2 Cells

1Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Chungbuk 28116, Republic of Korea
2College of Pharmacy, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea
3Department of Biology Education, Daegu University, Gyeongsan-si, Gyeongsangbuk 38453, Republic of Korea

Correspondence should be addressed to Dong-Oh Moon;, Hyun-Sun Lee;, and Mun-Ock Kim;

Received 4 September 2017; Revised 1 November 2017; Accepted 27 November 2017; Published 8 January 2018

Academic Editor: Shao-Hsuan Kao

Copyright © 2018 Eun-Bin Kwon et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Zanthoxylum ailanthoides (ZA) has been used as folk medicines in East Asian and recently reported to have several bioactivity; however, the studies of ZA on the regulation of triacylglycerol (TG) biosynthesis have not been elucidated yet. In this study, we examined whether the methanol extract of ZA (ZA-M) could reduce oleic acid- (OA-) induced intracellular lipid accumulation and confirmed its mode of action in HepG2 cells. ZA-M was shown to promote the phosphorylation of AMPK and its upstream LKB1, followed by reduction of lipogenic gene expressions. As a result, treatment of ZA-M blocked de novo TG biosynthesis and subsequently mitigated intracellular neutral lipid accumulation in HepG2 cells. ZA-M also inhibited OA-induced production of reactive oxygen species (ROS) and TNF-α, suggesting that ZA-M possess the anti-inflammatory feature in fatty acid over accumulated condition. Taken together, these results suggest that ZA-M attenuates OA-induced lipid accumulation and inflammation through the activation of LKB1/AMPK signaling pathway in HepG2 cells.