Polyphenol-Rich Extracts from Toona sinensis Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways
Identifieur interne : 000668 ( Pmc/Curation ); précédent : 000667; suivant : 000669Polyphenol-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
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DOI: 10.3390/jcm8101664
PubMed: 31614650
PubMed Central: 6832244
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">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><affiliation><nlm:aff id="af1-jcm-08-01664">Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan;<email>sshin810512@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-jcm-08-01664">Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708</wicri:regionArea></affiliation></author><author><name sortKey="Chen, Hsin Ju" sort="Chen, Hsin Ju" uniqKey="Chen H" first="Hsin-Ju" last="Chen">Hsin-Ju Chen</name><affiliation><nlm:aff id="af1-jcm-08-01664">Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan;<email>sshin810512@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-jcm-08-01664">Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708</wicri:regionArea></affiliation></author><author><name sortKey="Huang, Bu Miin" sort="Huang, Bu Miin" uniqKey="Huang B" first="Bu-Miin" last="Huang">Bu-Miin Huang</name><affiliation><nlm:aff id="af3-jcm-08-01664">Department of Anatomy, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan;<email>bumiin@mail.ncku.edu.tw</email></nlm:aff></affiliation></author><author><name sortKey="Chen, Yu Chi" sort="Chen, Yu Chi" uniqKey="Chen Y" first="Yu-Chi" last="Chen">Yu-Chi Chen</name><affiliation><nlm:aff id="af4-jcm-08-01664">Department of Urology, E-Da Hospital, Kaohsiung 82445, Taiwan;<email>yuchichen1978@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-jcm-08-01664">Department of Urology, E-Da Cancer Hospital, Kaohsiung 40402, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Urology, E-Da Cancer Hospital, Kaohsiung 40402</wicri:regionArea></affiliation></author><author><name sortKey="Chang, Chi Fen" sort="Chang, Chi Fen" uniqKey="Chang C" first="Chi-Fen" last="Chang">Chi-Fen Chang</name><affiliation><nlm:aff id="af6-jcm-08-01664">Department of Anatomy, School of Medicine, China Medical University, Taichung 40401, Taiwan;<email>cfchang@mail.cmu.edu.tw</email></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31614650</idno><idno type="pmc">6832244</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6832244</idno><idno type="RBID">PMC:6832244</idno><idno type="doi">10.3390/jcm8101664</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000668</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000668</idno><idno type="wicri:Area/Pmc/Curation">000668</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000668</idno></publicationStmt><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><affiliation><nlm:aff id="af1-jcm-08-01664">Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan;<email>sshin810512@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-jcm-08-01664">Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708</wicri:regionArea></affiliation></author><author><name sortKey="Chen, Hsin Ju" sort="Chen, Hsin Ju" uniqKey="Chen H" first="Hsin-Ju" last="Chen">Hsin-Ju Chen</name><affiliation><nlm:aff id="af1-jcm-08-01664">Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan;<email>sshin810512@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-jcm-08-01664">Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708</wicri:regionArea></affiliation></author><author><name sortKey="Huang, Bu Miin" sort="Huang, Bu Miin" uniqKey="Huang B" first="Bu-Miin" last="Huang">Bu-Miin Huang</name><affiliation><nlm:aff id="af3-jcm-08-01664">Department of Anatomy, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan;<email>bumiin@mail.ncku.edu.tw</email></nlm:aff></affiliation></author><author><name sortKey="Chen, Yu Chi" sort="Chen, Yu Chi" uniqKey="Chen Y" first="Yu-Chi" last="Chen">Yu-Chi Chen</name><affiliation><nlm:aff id="af4-jcm-08-01664">Department of Urology, E-Da Hospital, Kaohsiung 82445, Taiwan;<email>yuchichen1978@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-jcm-08-01664">Department of Urology, E-Da Cancer Hospital, Kaohsiung 40402, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Urology, E-Da Cancer Hospital, Kaohsiung 40402</wicri:regionArea></affiliation></author><author><name sortKey="Chang, Chi Fen" sort="Chang, Chi Fen" uniqKey="Chang C" first="Chi-Fen" last="Chang">Chi-Fen Chang</name><affiliation><nlm:aff id="af6-jcm-08-01664">Department of Anatomy, School of Medicine, China Medical University, Taichung 40401, Taiwan;<email>cfchang@mail.cmu.edu.tw</email></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Clinical Medicine</title><idno type="eISSN">2077-0383</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Dyson, J K" uniqKey="Dyson J">J.K. Dyson</name></author><author><name sortKey="Anstee, Q M" uniqKey="Anstee Q">Q.M. Anstee</name></author><author><name sortKey="Mcpherson, S" uniqKey="Mcpherson S">S. McPherson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Anstee, Q M" uniqKey="Anstee Q">Q.M. Anstee</name></author><author><name sortKey="Targher, G" uniqKey="Targher G">G. Targher</name></author><author><name sortKey="Day, C P" uniqKey="Day C">C.P. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Med</journal-id><journal-id journal-id-type="iso-abbrev">J Clin Med</journal-id><journal-id journal-id-type="publisher-id">jcm</journal-id><journal-title-group><journal-title>Journal of Clinical Medicine</journal-title></journal-title-group><issn pub-type="epub">2077-0383</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31614650</article-id><article-id pub-id-type="pmc">6832244</article-id><article-id pub-id-type="doi">10.3390/jcm8101664</article-id><article-id pub-id-type="publisher-id">jcm-08-01664</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Polyphenol-Rich Extracts from <italic>Toona sinensis</italic> Bark and Fruit Ameliorate Free Fatty Acid-Induced Lipogenesis through AMPK and LC3 Pathways</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-1953-4614</contrib-id><name><surname>Chen</surname><given-names>Yung-Chia</given-names></name><xref ref-type="aff" rid="af1-jcm-08-01664">1</xref><xref ref-type="aff" rid="af2-jcm-08-01664">2</xref><xref rid="c1-jcm-08-01664" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Hsin-Ju</given-names></name><xref ref-type="aff" rid="af1-jcm-08-01664">1</xref><xref ref-type="aff" rid="af2-jcm-08-01664">2</xref></contrib><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Bu-Miin</given-names></name><xref ref-type="aff" rid="af3-jcm-08-01664">3</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Yu-Chi</given-names></name><xref ref-type="aff" rid="af4-jcm-08-01664">4</xref><xref ref-type="aff" rid="af5-jcm-08-01664">5</xref></contrib><contrib contrib-type="author"><name><surname>Chang</surname><given-names>Chi-Fen</given-names></name><xref ref-type="aff" rid="af6-jcm-08-01664">6</xref></contrib></contrib-group><aff id="af1-jcm-08-01664"><label>1</label>Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan;<email>sshin810512@gmail.com</email></aff><aff id="af2-jcm-08-01664"><label>2</label>Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan</aff><aff id="af3-jcm-08-01664"><label>3</label>Department of Anatomy, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan;<email>bumiin@mail.ncku.edu.tw</email></aff><aff id="af4-jcm-08-01664"><label>4</label>Department of Urology, E-Da Hospital, Kaohsiung 82445, Taiwan;<email>yuchichen1978@gmail.com</email></aff><aff id="af5-jcm-08-01664"><label>5</label>Department of Urology, E-Da Cancer Hospital, Kaohsiung 40402, Taiwan</aff><aff id="af6-jcm-08-01664"><label>6</label>Department of Anatomy, School of Medicine, China Medical University, Taichung 40401, Taiwan;<email>cfchang@mail.cmu.edu.tw</email></aff><author-notes><corresp id="c1-jcm-08-01664"><label>*</label>Correspondence: <email>yungchia@kmu.edu.tw</email>; Tel.: +886-7-312-1101</corresp></author-notes><pub-date pub-type="epub"><day>11</day><month>10</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>10</month><year>2019</year></pub-date><volume>8</volume><issue>10</issue><elocation-id>1664</elocation-id><history><date date-type="received"><day>26</day><month>8</month><year>2019</year></date><date date-type="accepted"><day>03</day><month>10</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>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 (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><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></abstract><kwd-group><kwd><italic>Toona sinensis</italic></kwd><kwd>lipid accumulation</kwd><kwd>lipogenesis</kwd><kwd>LC3</kwd><kwd>AMPK</kwd><kwd>HepG2</kwd></kwd-group></article-meta></front><floats-group><fig id="jcm-08-01664-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>LC–MS analysis of <italic>T. sinensis</italic> leaves, root, or bark (TSB) and <italic>T. sinensis</italic> fruit (TSF) extracts. (<bold>A</bold>) Gallic acid, (<bold>B</bold>) rutin, (<bold>C</bold>) quercetin, and (<bold>D</bold>) toosendanin.</p></caption><graphic xlink:href="jcm-08-01664-g001"></graphic></fig><fig id="jcm-08-01664-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Effects of free fatty acids (FFAs) mixture on lipid accumulation and cytotoxicity in HepG2 cells. (<bold>A</bold>) Oil Red O staining. (<bold>B</bold>) Quantification of lipid contents. (<bold>C</bold>) MTT assays. The representative images are from six independent experiments. Scale bar: 50 μm. Data were quantified for three to six independent experiments and expressed as mean ± SD. * <italic>P</italic> < 0.05 compared with the control group (0 mM).</p></caption><graphic xlink:href="jcm-08-01664-g002"></graphic></fig><fig id="jcm-08-01664-f003" orientation="portrait" position="float"><label>Figure 3</label><caption><p>Effects of TSB and TSF extracts on lipid accumulation and cytotoxicity in HepG2 cells. (<bold>A</bold>) Oil Red O staining. Scale bar = 50 μm. The representative images are from eight independent experiments. (<bold>B</bold> and <bold>C</bold>) Quantification of lipid contents. (<bold>D</bold>–<bold>F</bold>) MTT assays. Data were quantified for three to twelve independent experiments and expressed as mean ± SD. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (0 g/mL). * <italic>P</italic> < 0.05 compared with the FFA group. In B–D, *** <italic>P</italic> < 0.001. In <xref ref-type="fig" rid="jcm-08-01664-f003">Figure 3</xref>F, ** <italic>P</italic> < 0.01, *** <italic>P</italic> < 0.001 compared with contro (0 μM).</p></caption><graphic xlink:href="jcm-08-01664-g003"></graphic></fig><fig id="jcm-08-01664-f004" orientation="portrait" position="float"><label>Figure 4</label><caption><p>Effects of TSB (<bold>A</bold>) and TSF (<bold>B</bold>) extracts on FFA-induced intracellular triglyceride levels. Fenofibrate (Feno, 125 μM) was used as a positive control. In renal carcinoma cells, 786-O served as a negative control. The bar graphs show the quantification of the triglyceride contents. Data from six independent experiments are expressed as mean ± SD. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (con). * <italic>P</italic> < 0.05, ** <italic>P</italic> < 0.01, *** <italic>P</italic> < 0.001 compared with the FFA group. (please add the sentence after * <italic>P</italic> < 0.05.</p></caption><graphic xlink:href="jcm-08-01664-g004"></graphic></fig><fig id="jcm-08-01664-f005" orientation="portrait" position="float"><label>Figure 5</label><caption><p>Effects of TSB and TSF extracts on FFA-induced lipogenic protein expression. (<bold>A</bold> and <bold>B</bold>) Immunoblots of lipogenic protein expression in TSB and TSF pre-treated lipid-laden HepG2 cells. GAPDH was used as the internal control. (<bold>C</bold>–<bold>L</bold>) The bar graphs show densitometric data (mean ± SD) from three to eight independent experiments. The images shown represent one experiment. <sup>#</sup><italic>P</italic> < 0.05 and <sup>##</sup> P < 0.01 compared with the control group (con). * <italic>P</italic> < 0.05, ** <italic>P</italic> < 0.01 and *** <italic>P</italic> < 0.001 compared with the FFA group.</p></caption><graphic xlink:href="jcm-08-01664-g005"></graphic></fig><fig id="jcm-08-01664-f006" orientation="portrait" position="float"><label>Figure 6</label><caption><p>TSB and TSF extracts’ effects on AMPK activation in HepG2 cells. (<bold>A</bold>–<bold>D</bold>) Immunoblots of phosphorylated AMPK expression in HepG2 cells. Total AMPK and GAPDH were used as the internal control. (<bold>E</bold>–<bold>H</bold>) The bar graphs show densitometric data (mean ± SD) from three to ten independent experiments. (<bold>I</bold>) Oil Red O staining. (<bold>J</bold> and <bold>K</bold>) Quantification of lipid contents. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (0 h). * <italic>P</italic> < 0.05 compared with the FFA group. ** <italic>P</italic> < 0.01 and *** <italic>P</italic> < 0.001 compared with the FFA group. Scale bar = 50 μm.</p></caption><graphic xlink:href="jcm-08-01664-g006"></graphic></fig><fig id="jcm-08-01664-f007" orientation="portrait" position="float"><label>Figure 7</label><caption><p>TSB and TSF’s effects on phosphorylated AMPK and ACC expression in FFA-treated HepG2 cells. (<bold>A</bold> and <bold>B</bold>) Immunoblots of phosphorylated AMPK and ACC levels. AMPK, ACC and GAPDH were used as internal controls. (<bold>C</bold>–<bold>F</bold>) The bar graphs show densitometric data (mean ± SD) from three to ten independent experiments. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (con). * <italic>P</italic> < 0.05 and ** <italic>P</italic> < 0.01 compared with the FFA group. *** <italic>P</italic> < 0.001 compared with the FFA group.</p></caption><graphic xlink:href="jcm-08-01664-g007"></graphic></fig><fig id="jcm-08-01664-f008" orientation="portrait" position="float"><label>Figure 8</label><caption><p>TSB and TSF’s effects on PPARα expression in FFA-treated HepG2 cells. (<bold>A</bold> and <bold>B</bold>) Immunoblots of PPAR. (<bold>C</bold> and <bold>D</bold>) The bar graphs show densitometric data (mean ± SD) from three to five independent experiments. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (con). * <italic>P</italic> < 0.05 and ** <italic>P</italic> < 0.01 compared with the FFA group.</p></caption><graphic xlink:href="jcm-08-01664-g008"></graphic></fig><fig id="jcm-08-01664-f009" orientation="portrait" position="float"><label>Figure 9</label><caption><p>Effects of TSB and TSF on autophagic flux in HepG2 cells. (<bold>A</bold>–<bold>D</bold>) Immunoblots of LC3 subunits. (<bold>E</bold>–<bold>H</bold>) The bar graphs show densitometric data (mean ± SD) from three to five independent experiments. (<bold>I</bold>) Oil Red O staining. (<bold>J</bold> and <bold>K</bold>) Quantification of lipid contents. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (con). * <italic>P</italic> < 0.05 and ** <italic>P</italic> < 0.01 compared with the FFA group. Scale bar = 50 μm.</p></caption><graphic xlink:href="jcm-08-01664-g009"></graphic></fig><fig id="jcm-08-01664-f010" orientation="portrait" position="float"><label>Figure 10</label><caption><p>Effects of TSB and TSF on the LC3 pathway in FFA-treated HepG2 cells. (<bold>A</bold> and <bold>B</bold>) Immunoblots of phosphorylated ULK and LC3 subunits. (<bold>C</bold>–<bold>F</bold>) The bar graphs show densitometric data (mean ± SD) from three to five independent experiments. <sup>#</sup><italic>P</italic> < 0.05 compared with the control group (con). * <italic>P</italic> < 0.05 and ** <italic>P</italic> < 0.01 compared with the FFA group.</p></caption><graphic xlink:href="jcm-08-01664-g010"></graphic></fig><fig id="jcm-08-01664-f011" orientation="portrait" position="float"><label>Figure 11</label><caption><p>Effects of compounds isolated from <italic>T. sinensis</italic> on lipid accumulation in HepG2 cells. (<bold>A</bold>–<bold>D</bold>) Nile red staining. Data were quantified for three to eight independent experiments and expressed as mean ± SD. <sup>##</sup><italic>P</italic> < 0.01 compared with the control group (con). * <italic>P</italic> < 0.05 and ** <italic>P</italic> < 0.01 compared with the FFA group.</p></caption><graphic xlink:href="jcm-08-01664-g011"></graphic></fig><table-wrap id="jcm-08-01664-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">jcm-08-01664-t001_Table 1</object-id><label>Table 1</label><caption><p>List of antibodies.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Antibody</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Dilution</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Brand</th></tr></thead><tbody><tr><td align="center" valign="middle" rowspan="1" colspan="1">FASN, <italic>p</italic>-AMPK (Thr 172), AMPK, pACC (Ser79), ACC</td><td align="center" valign="middle" rowspan="1" colspan="1">1:1000</td><td align="center" valign="middle" rowspan="1" colspan="1">Cell Signaling Technology Inc. (Danvers, MA, USA)</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">SREBP-1c, PPARα, SCD1</td><td align="center" valign="middle" rowspan="1" colspan="1">1:1000</td><td align="center" valign="middle" rowspan="1" colspan="1">Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA)</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">LXR<break></break>GAPDH</td><td align="center" valign="middle" rowspan="1" colspan="1">1:1000<break></break>1:3000</td><td align="center" valign="middle" rowspan="1" colspan="1">Proteintech Group Inc. (Rosemont, IL, USA)</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LC3B</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">1:1000</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Novus Biologicals, LLC., a Bio-Techne brand (Centennial, CO, USA)</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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