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

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,...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5672637/
https://www.ncbi.nlm.nih.gov/pubmed/29201040
http://dx.doi.org/10.1155/2017/3912567
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author 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
author_facet 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
author_sort Lee, Yong-Jik
collection PubMed
description 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.
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spelling pubmed-56726372017-12-03 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 PPAR Res Research Article 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. Hindawi 2017 2017-10-23 /pmc/articles/PMC5672637/ /pubmed/29201040 http://dx.doi.org/10.1155/2017/3912567 Text en Copyright © 2017 Yong-Jik Lee et al. https://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Research Article
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
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
title_full Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice
title_fullStr Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice
title_full_unstemmed Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice
title_short Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPARδ and Adiponectin in ApoE KO Mice
title_sort caffeoylquinic acid-rich extract of aster glehni f. schmidt ameliorates nonalcoholic fatty liver through the regulation of pparδ and adiponectin in apoe ko mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5672637/
https://www.ncbi.nlm.nih.gov/pubmed/29201040
http://dx.doi.org/10.1155/2017/3912567
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