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PPAR Research
Volume 2017, Article ID 3912567, 19 pages
Research Article

Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice

1Cardiovascular Center, Korea University, Guro Hospital, 148 Gurodong-ro, Guro-gu, Seoul 08308, Republic of Korea
2Department of Medical Science, Korea University College of Medicine (BK21 Plus KUMS Graduate Program), Main Building 6F Room 655, 73 Inchon-ro (Anam-dong 5-ga), Seongbuk-gu, Seoul 136-705, Republic of Korea
3Molecular Recognition Research Center, Materials and Life Science Research Division, Korea Institute of Science and Technology, Hwarangno 14 Gil 5, Seoul 136-791, Republic of Korea

Correspondence should be addressed to Hyoung Ja Kim; and Hong Seog Seo; rk.oc.letinu@oesshdm

Received 11 April 2017; Revised 4 June 2017; Accepted 10 September 2017; Published 23 October 2017

Academic Editor: Henrike Sell

Copyright © 2017 Yong-Jik Lee 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.


Aster glehni is well known for its therapeutic properties. This study was performed to investigate the effects of A. glehni on nonalcoholic fatty liver disease (NAFLD) in atherosclerotic condition, by determining the levels of biomarkers related to lipid metabolism and inflammation in serum, liver, and adipose tissue. Body and abdominal adipose tissue weights and serum triglyceride level decreased in all groups treated with A. glehni. Serum adiponectin concentration and protein levels of peroxisome proliferator-activated receptor δ, 5′ adenosine monophosphate-activated protein kinase, acetyl-CoA carboxylase, superoxide dismutase, and PPARγ coactivator 1-alpha in liver tissues increased in the groups treated with A. glehni. Conversely, protein levels of ATP citrate lyase, fatty acid synthase, tumor necrosis factor α, and 3-hydroxy-3-methylglutaryl-CoA reductase and the concentrations of interleukin 6 and reactive oxygen species decreased upon A. glehni. Triglyceride concentration in the liver was lower in mice treated with A. glehni than in control mice. Lipid accumulation in HepG2 and 3T3-L1 cells decreased upon A. glehni treatment; this effect was suppressed in the presence of the PPARδ antagonist, GSK0660. Our findings suggest that A. glehni extracts may ameliorate NAFLD through regulation of PPARδ, adiponectin, and the related subgenes.