Polyphenol-Rich Extracts from Toona sinensis Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways
Identifieur interne : 000529 ( Main/Exploration ); précédent : 000528; suivant : 000530Polyphenol-Rich Extracts from Toona sinensis Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways
Auteurs : Yung-Chia Chen [Taïwan] ; Hsin-Ju Chen [Taïwan] ; Bu-Miin Huang ; Yu-Chi Chen [Taïwan] ; Chi-Fen ChangSource :
- Journal of Clinical Medicine [ 2077-0383 ] ; 2019.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease found worldwide. The present study aimed to evaluate the mechanisms of inhibiting lipid accumulation in free fatty acid (FFA)-treated HepG2 cells caused by bark and fruit extracts of
Url:
DOI: 10.3390/jcm8101664
PubMed: 31614650
PubMed Central: 6832244
Affiliations:
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Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways</title>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Polyphenol-Rich Extracts from <italic>Toona sinensis</italic>
Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways</title>
<author><name sortKey="Chen, Yung Chia" sort="Chen, Yung Chia" uniqKey="Chen Y" first="Yung-Chia" last="Chen">Yung-Chia Chen</name>
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<author><name sortKey="Chen, Hsin Ju" sort="Chen, Hsin Ju" uniqKey="Chen H" first="Hsin-Ju" last="Chen">Hsin-Ju Chen</name>
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<author><name sortKey="Chang, Chi Fen" sort="Chang, Chi Fen" uniqKey="Chang C" first="Chi-Fen" last="Chang">Chi-Fen Chang</name>
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<series><title level="j">Journal of Clinical Medicine</title>
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<front><div type="abstract" xml:lang="en"><p>Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease found worldwide. The present study aimed to evaluate the mechanisms of inhibiting lipid accumulation in free fatty acid (FFA)-treated HepG2 cells caused by bark and fruit extracts of <italic>Toona sinensis</italic>
(TSB and TSF). FFA induced lipid and triglyceride (TG) accumulation, which was attenuated by TSB and TSF. TSB and/or TSF promoted phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-coA carboxylase and peroxisome proliferator-activated receptor alpha upregulation. Furthermore, TSB and TSF suppressed FFA-induced liver X receptor, sterol regulatory element-binding transcription protein 1, fatty acid synthase, and stearoyl-CoA desaturase 1 protein expression. Moreover, TSB and/or TSF induced phosphorylation of Unc-51 like autophagy-activating kinase and microtubule-associated protein 1A/1B-light chain 3 expressions. Therefore, TSB and TSF relieve lipid accumulation by attenuating lipogenic protein expression, activating the AMPK pathway, and upregulating the autophagic flux to enhance lipid metabolism. Moreover, TSB and TSF reduced TG contents, implying the therapeutic use of TSB and TSF in NAFLD.</p>
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