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Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells

Liver metabolic disorders and oxidative stress are crucial factors in the development of nonalcoholic fatty liver disease (NAFLD); however, treatment strategies to combat NAFLD remain poorly established, presenting an important challenge that needs to be addressed. Herein, we aimed to examine the ef...

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Autores principales: Kim, Sou Hyun, Yun, Chawon, Kwon, Doyoung, Lee, Yun-Hee, Kwak, Jae-Hwan, Jung, Young-Suk
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9919102/
https://www.ncbi.nlm.nih.gov/pubmed/36771140
http://dx.doi.org/10.3390/molecules28031476
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author Kim, Sou Hyun
Yun, Chawon
Kwon, Doyoung
Lee, Yun-Hee
Kwak, Jae-Hwan
Jung, Young-Suk
author_facet Kim, Sou Hyun
Yun, Chawon
Kwon, Doyoung
Lee, Yun-Hee
Kwak, Jae-Hwan
Jung, Young-Suk
author_sort Kim, Sou Hyun
collection PubMed
description Liver metabolic disorders and oxidative stress are crucial factors in the development of nonalcoholic fatty liver disease (NAFLD); however, treatment strategies to combat NAFLD remain poorly established, presenting an important challenge that needs to be addressed. Herein, we aimed to examine the effect of isoquercitrin on lipid accumulation induced by exogenous free fatty acids (FFA) using HepG2 cells and elucidate the underlying molecular mechanism. The cells were exposed to 0.5 mM FFA to induce intracellular lipid accumulation, followed by co-treatment with isoquercitrin to confirm the potential inhibitory effect on FFA-induced lipid production. HepG2 cells exposed to FFA alone exhibited intracellular lipid accumulation, compromised endoplasmic reticulum (ER) stress, and enhanced expression of proteins and genes involved in lipid synthesis; however, co-treatment with isoquercitrin decreased the expression of these molecules in a dose-dependent manner. Furthermore, isoquercitrin could activate AMP-activated protein kinase (AMPK), a key regulatory protein of hepatic fatty acid oxidation, suppressing new lipid production by phosphorylating acetyl-CoA carboxylase (ACC) and inhibiting sterol regulatory element-binding transcription factor 1 (SREBP-1)/fatty acid synthase (FAS) signals. Overall, these findings suggest that isoquercitrin can be employed as a therapeutic agent to improve NAFLD via the regulation of lipid metabolism by targeting the AMPK/ACC and SREBP1/FAS pathways.
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spelling pubmed-99191022023-02-12 Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells Kim, Sou Hyun Yun, Chawon Kwon, Doyoung Lee, Yun-Hee Kwak, Jae-Hwan Jung, Young-Suk Molecules Article Liver metabolic disorders and oxidative stress are crucial factors in the development of nonalcoholic fatty liver disease (NAFLD); however, treatment strategies to combat NAFLD remain poorly established, presenting an important challenge that needs to be addressed. Herein, we aimed to examine the effect of isoquercitrin on lipid accumulation induced by exogenous free fatty acids (FFA) using HepG2 cells and elucidate the underlying molecular mechanism. The cells were exposed to 0.5 mM FFA to induce intracellular lipid accumulation, followed by co-treatment with isoquercitrin to confirm the potential inhibitory effect on FFA-induced lipid production. HepG2 cells exposed to FFA alone exhibited intracellular lipid accumulation, compromised endoplasmic reticulum (ER) stress, and enhanced expression of proteins and genes involved in lipid synthesis; however, co-treatment with isoquercitrin decreased the expression of these molecules in a dose-dependent manner. Furthermore, isoquercitrin could activate AMP-activated protein kinase (AMPK), a key regulatory protein of hepatic fatty acid oxidation, suppressing new lipid production by phosphorylating acetyl-CoA carboxylase (ACC) and inhibiting sterol regulatory element-binding transcription factor 1 (SREBP-1)/fatty acid synthase (FAS) signals. Overall, these findings suggest that isoquercitrin can be employed as a therapeutic agent to improve NAFLD via the regulation of lipid metabolism by targeting the AMPK/ACC and SREBP1/FAS pathways. MDPI 2023-02-03 /pmc/articles/PMC9919102/ /pubmed/36771140 http://dx.doi.org/10.3390/molecules28031476 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Sou Hyun
Yun, Chawon
Kwon, Doyoung
Lee, Yun-Hee
Kwak, Jae-Hwan
Jung, Young-Suk
Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title_full Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title_fullStr Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title_full_unstemmed Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title_short Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells
title_sort effect of isoquercitrin on free fatty acid-induced lipid accumulation in hepg2 cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9919102/
https://www.ncbi.nlm.nih.gov/pubmed/36771140
http://dx.doi.org/10.3390/molecules28031476
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