Corosolic Acid Attenuates Hepatic Lipid Accumulation and Inflammatory Response via AMPK/SREBPs and NF-κB/MAPK Signaling Pathways.
Identifieur interne : 000188 ( Main/Exploration ); précédent : 000187; suivant : 000189Corosolic Acid Attenuates Hepatic Lipid Accumulation and Inflammatory Response via AMPK/SREBPs and NF-κB/MAPK Signaling Pathways.
Auteurs : Jian-Xiu Zhang [République populaire de Chine] ; Wei-Jun Feng [République populaire de Chine] ; Guan-Cheng Liu [République populaire de Chine] ; Qian-Qian Ma [République populaire de Chine] ; Hai-Lan Li [République populaire de Chine] ; Xiao-Yan Gao [République populaire de Chine] ; Hui-Zhe Liu [République populaire de Chine] ; Guang-Chun Piao [République populaire de Chine] ; Hai-Dan Yuan [République populaire de Chine]Source :
- The American journal of Chinese medicine [ 1793-6853 ] ; 2020.
Descripteurs français
- KwdFr :
- Acyl-(acyl-carrier-protein)desaturase (métabolisme), Animaux (MeSH), Antigènes CD95 (métabolisme), Cellules HepG2 (MeSH), Facteur de transcription NF-kappa B (métabolisme), Foie (métabolisme), Humains (MeSH), Hyperlipidémies (traitement médicamenteux), Hypolipémiants (MeSH), Inflammation (MeSH), Lagerstroemia (composition chimique), Métabolisme lipidique (effets des médicaments et des substances chimiques), Phytothérapie (MeSH), Souris de lignée ICR (MeSH), Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques), Triterpènes (pharmacologie), Triterpènes (usage thérapeutique).
- MESH :
- composition chimique : Lagerstroemia.
- effets des médicaments et des substances chimiques : Métabolisme lipidique, Système de signalisation des MAP kinases.
- métabolisme : Acyl-(acyl-carrier-protein)desaturase, Antigènes CD95, Facteur de transcription NF-kappa B, Foie.
- pharmacologie : Triterpènes.
- traitement médicamenteux : Hyperlipidémies.
- usage thérapeutique : Triterpènes.
- Animaux, Cellules HepG2, Humains, Hypolipémiants, Inflammation, Phytothérapie, Souris de lignée ICR.
English descriptors
- KwdEn :
- Animals (MeSH), Hep G2 Cells (MeSH), Humans (MeSH), Hyperlipidemias (drug therapy), Hypolipidemic Agents (MeSH), Inflammation (MeSH), Lagerstroemia (chemistry), Lipid Metabolism (drug effects), Liver (metabolism), MAP Kinase Signaling System (drug effects), Mice, Inbred ICR (MeSH), NF-kappa B (metabolism), Phytotherapy (MeSH), Stearoyl-CoA Desaturase (metabolism), Triterpenes (pharmacology), Triterpenes (therapeutic use), fas Receptor (metabolism).
- MESH :
- chemical , metabolism : NF-kappa B, Stearoyl-CoA Desaturase, fas Receptor.
- chemical , pharmacology : Triterpenes.
- chemical , therapeutic use : Triterpenes.
- chemical : Hypolipidemic Agents.
- chemistry : Lagerstroemia.
- drug effects : Lipid Metabolism, MAP Kinase Signaling System.
- drug therapy : Hyperlipidemias.
- metabolism : Liver.
- Animals, Hep G2 Cells, Humans, Inflammation, Mice, Inbred ICR, Phytotherapy.
Abstract
Corosolic acid (CA) is the main active component of Lagetstroemia speciosa and has been known to serve as several different pharmacological effects, such as antidiabetic, anti-oxidant, and anticancer effects. In this study, effects of CA on the hepatic lipid accumulation were examined using HepG2 cells and tyloxapol (TY)-induced hyperlipidemia ICR mice. CA significantly inhibited hepatic lipid accumulation via inhibition of SREBPs, and its target genes FAS, SCD1, and HMGCR transcription in HepG2 cells. These effects were mediated through activation of AMPK, and these effects were all abolished in the presence of compound C (CC, an AMPK inhibitor). In addition, CA clearly alleviated serum ALT, AST, TG, TC, low-density lipoprotein cholesterol (LDL-C), and increased high-density lipoprotein cholesterol (HDL-C) levels, and obviously attenuated TY-induced liver steatosis and inflammation. Moreover, CA significantly upregulated AMPK, ACC, LKB1 phosphorylation, and significantly inhibited lipin1, SREBPs, TNF-α κ κ
DOI: 10.1142/S0192415X20500299
PubMed: 32329643
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province</wicri:regionArea><wicri:noRegion>Jilin Province</wicri:noRegion></affiliation></author></analytic><series><title level="j">The American journal of Chinese medicine</title><idno type="eISSN">1793-6853</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Hep G2 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Hyperlipidemias (drug therapy)</term><term>Hypolipidemic Agents (MeSH)</term><term>Inflammation (MeSH)</term><term>Lagerstroemia (chemistry)</term><term>Lipid Metabolism (drug effects)</term><term>Liver (metabolism)</term><term>MAP Kinase Signaling System (drug effects)</term><term>Mice, Inbred ICR (MeSH)</term><term>NF-kappa B (metabolism)</term><term>Phytotherapy (MeSH)</term><term>Stearoyl-CoA Desaturase (metabolism)</term><term>Triterpenes (pharmacology)</term><term>Triterpenes (therapeutic use)</term><term>fas Receptor (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acyl-(acyl-carrier-protein)desaturase (métabolisme)</term><term>Animaux (MeSH)</term><term>Antigènes CD95 (métabolisme)</term><term>Cellules HepG2 (MeSH)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Foie (métabolisme)</term><term>Humains (MeSH)</term><term>Hyperlipidémies (traitement médicamenteux)</term><term>Hypolipémiants (MeSH)</term><term>Inflammation (MeSH)</term><term>Lagerstroemia (composition chimique)</term><term>Métabolisme lipidique (effets des médicaments et des substances chimiques)</term><term>Phytothérapie (MeSH)</term><term>Souris de lignée ICR (MeSH)</term><term>Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques)</term><term>Triterpènes (pharmacologie)</term><term>Triterpènes (usage thérapeutique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term><term>Stearoyl-CoA Desaturase</term><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Triterpenes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Triterpenes</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Hypolipidemic Agents</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Lagerstroemia</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Lagerstroemia</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lipid Metabolism</term><term>MAP Kinase Signaling System</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Hyperlipidemias</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Métabolisme lipidique</term><term>Système de signalisation des MAP kinases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Liver</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acyl-(acyl-carrier-protein)desaturase</term><term>Antigènes CD95</term><term>Facteur de transcription NF-kappa B</term><term>Foie</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Triterpènes</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Hyperlipidémies</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Triterpènes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Hep G2 Cells</term><term>Humans</term><term>Inflammation</term><term>Mice, Inbred ICR</term><term>Phytotherapy</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HepG2</term><term>Humains</term><term>Hypolipémiants</term><term>Inflammation</term><term>Phytothérapie</term><term>Souris de lignée ICR</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Corosolic acid (CA) is the main active component of <i>Lagetstroemia speciosa</i> and has been known to serve as several different pharmacological effects, such as antidiabetic, anti-oxidant, and anticancer effects. In this study, effects of CA on the hepatic lipid accumulation were examined using HepG2 cells and tyloxapol (TY)-induced hyperlipidemia ICR mice. CA significantly inhibited hepatic lipid accumulation via inhibition of SREBPs, and its target genes FAS, SCD1, and HMGCR transcription in HepG2 cells. These effects were mediated through activation of AMPK, and these effects were all abolished in the presence of compound C (CC, an AMPK inhibitor). In addition, CA clearly alleviated serum ALT, AST, TG, TC, low-density lipoprotein cholesterol (LDL-C), and increased high-density lipoprotein cholesterol (HDL-C) levels, and obviously attenuated TY-induced liver steatosis and inflammation. Moreover, CA significantly upregulated AMPK, ACC, LKB1 phosphorylation, and significantly inhibited lipin1, SREBPs, TNF-<mml:math><mml:mi>α</mml:mi></mml:math>, F4/80, caspase-1 expression, NF-<mml:math><mml:mi>κ</mml:mi></mml:math>B translocation, and MAPK activation in TY-induced hyperlipidemia mice. Our results suggest that CA is a potent antihyperlipidemia and antihepatic steatosis agent and the mechanism involved both lipogenesis and cholesterol synthesis and inflammation response inhibition via AMPK/SREBPs and NF-<mml:math><mml:mi>κ</mml:mi></mml:math>B/MAPK signaling pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32329643</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>08</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1793-6853</ISSN><JournalIssue CitedMedium="Internet"><Volume>48</Volume><Issue>3</Issue><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>The American journal of Chinese medicine</Title><ISOAbbreviation>Am J Chin Med</ISOAbbreviation></Journal><ArticleTitle>Corosolic Acid Attenuates Hepatic Lipid Accumulation and Inflammatory Response via AMPK/SREBPs and NF-<mml:math><mml:mi>κ</mml:mi></mml:math>B/MAPK Signaling Pathways.</ArticleTitle><Pagination><MedlinePgn>579-595</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1142/S0192415X20500299</ELocationID><Abstract><AbstractText>Corosolic acid (CA) is the main active component of <i>Lagetstroemia speciosa</i> and has been known to serve as several different pharmacological effects, such as antidiabetic, anti-oxidant, and anticancer effects. In this study, effects of CA on the hepatic lipid accumulation were examined using HepG2 cells and tyloxapol (TY)-induced hyperlipidemia ICR mice. CA significantly inhibited hepatic lipid accumulation via inhibition of SREBPs, and its target genes FAS, SCD1, and HMGCR transcription in HepG2 cells. These effects were mediated through activation of AMPK, and these effects were all abolished in the presence of compound C (CC, an AMPK inhibitor). In addition, CA clearly alleviated serum ALT, AST, TG, TC, low-density lipoprotein cholesterol (LDL-C), and increased high-density lipoprotein cholesterol (HDL-C) levels, and obviously attenuated TY-induced liver steatosis and inflammation. Moreover, CA significantly upregulated AMPK, ACC, LKB1 phosphorylation, and significantly inhibited lipin1, SREBPs, TNF-<mml:math><mml:mi>α</mml:mi></mml:math>, F4/80, caspase-1 expression, NF-<mml:math><mml:mi>κ</mml:mi></mml:math>B translocation, and MAPK activation in TY-induced hyperlipidemia mice. Our results suggest that CA is a potent antihyperlipidemia and antihepatic steatosis agent and the mechanism involved both lipogenesis and cholesterol synthesis and inflammation response inhibition via AMPK/SREBPs and NF-<mml:math><mml:mi>κ</mml:mi></mml:math>B/MAPK signaling pathways.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jian-Xiu</ForeName><Initials>JX</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Wei-Jun</ForeName><Initials>WJ</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Guan-Cheng</ForeName><Initials>GC</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Qian-Qian</ForeName><Initials>QQ</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Hai-Lan</ForeName><Initials>HL</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Xiao-Yan</ForeName><Initials>XY</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Hui-Zhe</ForeName><Initials>HZ</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piao</LastName><ForeName>Guang-Chun</ForeName><Initials>GC</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Hai-Dan</ForeName><Initials>HD</Initials><AffiliationInfo><Affiliation>Key Laboratory of Natural Resources of Changbai, Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, P. R. China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>Singapore</Country><MedlineTA>Am J Chin Med</MedlineTA><NlmUniqueID>7901431</NlmUniqueID><ISSNLinking>0192-415X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491899">Fas protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000960">Hypolipidemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014315">Triterpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019014">fas Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>AMX2I57A98</RegistryNumber><NameOfSubstance UI="C113861">corosolic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.19.1</RegistryNumber><NameOfSubstance UI="C490333">Scd1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.19.1</RegistryNumber><NameOfSubstance UI="D013230">Stearoyl-CoA Desaturase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006949" MajorTopicYN="N">Hyperlipidemias</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000960" MajorTopicYN="Y">Hypolipidemic Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D031563" MajorTopicYN="N">Lagerstroemia</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050356" MajorTopicYN="N">Lipid Metabolism</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008813" MajorTopicYN="N">Mice, Inbred ICR</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008517" MajorTopicYN="Y">Phytotherapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013230" MajorTopicYN="N">Stearoyl-CoA Desaturase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014315" MajorTopicYN="N">Triterpenes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019014" MajorTopicYN="N">fas Receptor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AMPK</Keyword><Keyword MajorTopicYN="N">Corosolic Acid</Keyword><Keyword MajorTopicYN="N">Hyperlipidemia</Keyword><Keyword MajorTopicYN="N">Inflammatory Response</Keyword><Keyword MajorTopicYN="N">Liver Steatosis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>4</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>4</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32329643</ArticleId><ArticleId IdType="doi">10.1142/S0192415X20500299</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Jian Xiu" sort="Zhang, Jian Xiu" uniqKey="Zhang J" first="Jian-Xiu" last="Zhang">Jian-Xiu Zhang</name></noRegion><name sortKey="Feng, Wei Jun" sort="Feng, Wei Jun" uniqKey="Feng W" first="Wei-Jun" last="Feng">Wei-Jun Feng</name><name sortKey="Gao, Xiao Yan" sort="Gao, Xiao Yan" uniqKey="Gao X" first="Xiao-Yan" last="Gao">Xiao-Yan Gao</name><name sortKey="Li, Hai Lan" sort="Li, Hai Lan" uniqKey="Li H" first="Hai-Lan" last="Li">Hai-Lan Li</name><name sortKey="Liu, Guan Cheng" sort="Liu, Guan Cheng" uniqKey="Liu G" first="Guan-Cheng" last="Liu">Guan-Cheng Liu</name><name sortKey="Liu, Hui Zhe" sort="Liu, Hui Zhe" uniqKey="Liu H" first="Hui-Zhe" last="Liu">Hui-Zhe Liu</name><name sortKey="Ma, Qian Qian" sort="Ma, Qian Qian" uniqKey="Ma Q" first="Qian-Qian" last="Ma">Qian-Qian Ma</name><name sortKey="Piao, Guang Chun" sort="Piao, Guang Chun" uniqKey="Piao G" first="Guang-Chun" last="Piao">Guang-Chun Piao</name><name sortKey="Yuan, Hai Dan" sort="Yuan, Hai Dan" uniqKey="Yuan H" first="Hai-Dan" last="Yuan">Hai-Dan Yuan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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