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

Yong Jik Lee, Yoo Na Jang, Yoon Mi Han, Hyun Min Kim, Jong Min Jeong, Min Jeoung Son, Chang Bae Jin, Hyoung Ja Kim, Hong Seog Seo

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number3912567
JournalPPAR Research
Volume2017
DOIs
Publication statusPublished - 2017 Jan 1

Fingerprint

Peroxisome Proliferator-Activated Receptors
Adiponectin
Apolipoproteins E
Liver
Triglycerides
Serum
ATP Citrate (pro-S)-Lyase
3T3-L1 Cells
Hydroxymethylglutaryl CoA Reductases
Acetyl-CoA Carboxylase
Fatty Acid Synthases
Abdominal Fat
Adenosine Monophosphate
Lipid Metabolism
Protein Kinases
Superoxide Dismutase
Adipose Tissue
Interleukin-6
Reactive Oxygen Species
Proteins

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology (medical)

Cite this

Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice. / Lee, Yong Jik; Jang, Yoo Na; Han, Yoon Mi; Kim, Hyun Min; Jeong, Jong Min; Son, Min Jeoung; Jin, Chang Bae; Kim, Hyoung Ja; Seo, Hong Seog.

In: PPAR Research, Vol. 2017, 3912567, 01.01.2017.

Research output: Contribution to journalArticle

Lee, Yong Jik ; Jang, Yoo Na ; Han, Yoon Mi ; Kim, Hyun Min ; Jeong, Jong Min ; Son, Min Jeoung ; Jin, Chang Bae ; Kim, Hyoung Ja ; Seo, Hong Seog. / Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice. In: PPAR Research. 2017 ; Vol. 2017.
@article{1e5912178b394d27ae0e13b63e42c944,
title = "Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice",
abstract = "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.",
author = "Lee, {Yong Jik} and Jang, {Yoo Na} and Han, {Yoon Mi} and Kim, {Hyun Min} and Jeong, {Jong Min} and Son, {Min Jeoung} and Jin, {Chang Bae} and Kim, {Hyoung Ja} and Seo, {Hong Seog}",
year = "2017",
month = "1",
day = "1",
doi = "10.1155/2017/3912567",
language = "English",
volume = "2017",
journal = "PPAR Research",
issn = "1687-4757",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice

AU - Lee, Yong Jik

AU - Jang, Yoo Na

AU - Han, Yoon Mi

AU - Kim, Hyun Min

AU - Jeong, Jong Min

AU - Son, Min Jeoung

AU - Jin, Chang Bae

AU - Kim, Hyoung Ja

AU - Seo, Hong Seog

PY - 2017/1/1

Y1 - 2017/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85042480289&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85042480289&partnerID=8YFLogxK

U2 - 10.1155/2017/3912567

DO - 10.1155/2017/3912567

M3 - Article

AN - SCOPUS:85042480289

VL - 2017

JO - PPAR Research

JF - PPAR Research

SN - 1687-4757

M1 - 3912567

ER -