Parishin from Gastrodia elata Extends the Lifespan of Yeast via Regulation of Sir2/Uth1/TOR Signaling Pathway.
Identifieur interne : 000A49 ( Main/Exploration ); précédent : 000A48; suivant : 000A50Parishin from Gastrodia elata Extends the Lifespan of Yeast via Regulation of Sir2/Uth1/TOR Signaling Pathway.
Auteurs : Yanfei Lin [République populaire de Chine] ; Yujuan Sun [République populaire de Chine] ; Yufang Weng [République populaire de Chine] ; Akira Matsuura [Japon] ; Lan Xiang [République populaire de Chine] ; Jianhua Qi [République populaire de Chine]Source :
- Oxidative medicine and cellular longevity [ 1942-0994 ] ; 2016.
Descripteurs français
- KwdFr :
- Espèces réactives de l'oxygène (métabolisme), Gastrodia (composition chimique), Glucosides (composition chimique), Glucosides (pharmacologie), Malonaldéhyde (métabolisme), Mutation (génétique), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (physiologie), Stress oxydatif (effets des médicaments et des substances chimiques), Superoxide dismutase (métabolisme), Transduction du signal (effets des médicaments et des substances chimiques), Viabilité microbienne (effets des médicaments et des substances chimiques).
- MESH :
- composition chimique : Gastrodia, Glucosides.
- effets des médicaments et des substances chimiques : Régulation de l'expression des gènes fongiques, Saccharomyces cerevisiae, Stress oxydatif, Transduction du signal, Viabilité microbienne.
- génétique : Mutation, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- métabolisme : Espèces réactives de l'oxygène, Malonaldéhyde, Protéines de Saccharomyces cerevisiae, Superoxide dismutase.
- pharmacologie : Glucosides.
- physiologie : Saccharomyces cerevisiae.
English descriptors
- KwdEn :
- Gastrodia (chemistry), Gene Expression Regulation, Fungal (drug effects), Glucosides (chemistry), Glucosides (pharmacology), Malondialdehyde (metabolism), Microbial Viability (drug effects), Mutation (genetics), Oxidative Stress (drug effects), Reactive Oxygen Species (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects), Superoxide Dismutase (metabolism).
- MESH :
- chemical , chemistry : Glucosides.
- chemistry : Gastrodia.
- drug effects : Gene Expression Regulation, Fungal, Microbial Viability, Oxidative Stress, Saccharomyces cerevisiae, Signal Transduction.
- genetics : Mutation, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Malondialdehyde, Reactive Oxygen Species, Saccharomyces cerevisiae Proteins, Superoxide Dismutase.
- chemical , pharmacology : Glucosides.
- physiology : Saccharomyces cerevisiae.
Abstract
Parishin is a phenolic glucoside isolated from Gastrodia elata, which is an important traditional Chinese medicine; this glucoside significantly extended the replicative lifespan of K6001 yeast at 3, 10, and 30 μM. To clarify its mechanism of action, assessment of oxidative stress resistance, superoxide dismutase (SOD) activity, malondialdehyde (MDA), and reactive oxygen species (ROS) assays, replicative lifespans of sod1, sod2, uth1, and skn7 yeast mutants, and real-time quantitative PCR (RT-PCR) analysis were conducted. The significant increase of cell survival rate in oxidative stress condition was observed in parishin-treated groups. Silent information regulator 2 (Sir2) gene expression and SOD activity were significantly increased after treating parishin in normal condition. Meanwhile, the levels of ROS and MDA in yeast were significantly decreased. The replicative lifespans of sod1, sod2, uth1, and skn7 mutants of K6001 yeast were not affected by parishin. We also found that parishin could decrease the gene expression of TORC1, ribosomal protein S26A (RPS26A), and ribosomal protein L9A (RPL9A) in the target of rapamycin (TOR) signaling pathway. Gene expression levels of RPS26A and RPL9A in uth1, as well as in uth1, sir2 double mutants, were significantly lower than those of the control group. Besides, TORC1 gene expression in uth1 mutant of K6001 yeast was inhibited significantly. These results suggested that parishin exhibited antiaging effects via regulation of Sir2/Uth1/TOR signaling pathway.
DOI: 10.1155/2016/4074690
PubMed: 27429709
PubMed Central: PMC4939362
Affiliations:
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(métabolisme)</term><term>Gastrodia (composition chimique)</term><term>Glucosides (composition chimique)</term><term>Glucosides (pharmacologie)</term><term>Malonaldéhyde (métabolisme)</term><term>Mutation (génétique)</term><term>Protéines de Saccharomyces cerevisiae (génétique)</term><term>Protéines de Saccharomyces cerevisiae (métabolisme)</term><term>Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Saccharomyces cerevisiae (physiologie)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Superoxide dismutase (métabolisme)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Viabilité microbienne (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Glucosides</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Gastrodia</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Gastrodia</term><term>Glucosides</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation, Fungal</term><term>Microbial Viability</term><term>Oxidative Stress</term><term>Saccharomyces cerevisiae</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Régulation de l'expression des gènes fongiques</term><term>Saccharomyces cerevisiae</term><term>Stress oxydatif</term><term>Transduction du signal</term><term>Viabilité microbienne</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Saccharomyces cerevisiae</term><term>Saccharomyces 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cerevisiae</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parishin is a phenolic glucoside isolated from Gastrodia elata, which is an important traditional Chinese medicine; this glucoside significantly extended the replicative lifespan of K6001 yeast at 3, 10, and 30 μM. To clarify its mechanism of action, assessment of oxidative stress resistance, superoxide dismutase (SOD) activity, malondialdehyde (MDA), and reactive oxygen species (ROS) assays, replicative lifespans of sod1, sod2, uth1, and skn7 yeast mutants, and real-time quantitative PCR (RT-PCR) analysis were conducted. The significant increase of cell survival rate in oxidative stress condition was observed in parishin-treated groups. Silent information regulator 2 (Sir2) gene expression and SOD activity were significantly increased after treating parishin in normal condition. Meanwhile, the levels of ROS and MDA in yeast were significantly decreased. The replicative lifespans of sod1, sod2, uth1, and skn7 mutants of K6001 yeast were not affected by parishin. We also found that parishin could decrease the gene expression of TORC1, ribosomal protein S26A (RPS26A), and ribosomal protein L9A (RPL9A) in the target of rapamycin (TOR) signaling pathway. Gene expression levels of RPS26A and RPL9A in uth1, as well as in uth1, sir2 double mutants, were significantly lower than those of the control group. Besides, TORC1 gene expression in uth1 mutant of K6001 yeast was inhibited significantly. These results suggested that parishin exhibited antiaging effects via regulation of Sir2/Uth1/TOR signaling pathway. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27429709</PMID><DateCompleted><Year>2017</Year><Month>03</Month><Day>13</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1942-0994</ISSN><JournalIssue CitedMedium="Internet"><Volume>2016</Volume><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Oxidative medicine and cellular longevity</Title><ISOAbbreviation>Oxid Med Cell Longev</ISOAbbreviation></Journal><ArticleTitle>Parishin from Gastrodia elata Extends the Lifespan of Yeast via Regulation of Sir2/Uth1/TOR Signaling Pathway.</ArticleTitle><Pagination><MedlinePgn>4074690</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1155/2016/4074690</ELocationID><Abstract><AbstractText>Parishin is a phenolic glucoside isolated from Gastrodia elata, which is an important traditional Chinese medicine; this glucoside significantly extended the replicative lifespan of K6001 yeast at 3, 10, and 30 μM. To clarify its mechanism of action, assessment of oxidative stress resistance, superoxide dismutase (SOD) activity, malondialdehyde (MDA), and reactive oxygen species (ROS) assays, replicative lifespans of sod1, sod2, uth1, and skn7 yeast mutants, and real-time quantitative PCR (RT-PCR) analysis were conducted. The significant increase of cell survival rate in oxidative stress condition was observed in parishin-treated groups. Silent information regulator 2 (Sir2) gene expression and SOD activity were significantly increased after treating parishin in normal condition. Meanwhile, the levels of ROS and MDA in yeast were significantly decreased. The replicative lifespans of sod1, sod2, uth1, and skn7 mutants of K6001 yeast were not affected by parishin. We also found that parishin could decrease the gene expression of TORC1, ribosomal protein S26A (RPS26A), and ribosomal protein L9A (RPL9A) in the target of rapamycin (TOR) signaling pathway. Gene expression levels of RPS26A and RPL9A in uth1, as well as in uth1, sir2 double mutants, were significantly lower than those of the control group. Besides, TORC1 gene expression in uth1 mutant of K6001 yeast was inhibited significantly. These results suggested that parishin exhibited antiaging effects via regulation of Sir2/Uth1/TOR signaling pathway. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Yanfei</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Pharmaceutical Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yujuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Pharmaceutical Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weng</LastName><ForeName>Yufang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Pharmaceutical Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsuura</LastName><ForeName>Akira</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2300-7227</Identifier><AffiliationInfo><Affiliation>Department of Nanobiology, Graduate School of Advanced Integration Science, Chiba University, Chiba 263-8522, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiang</LastName><ForeName>Lan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>College of Pharmaceutical Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qi</LastName><ForeName>Jianhua</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Pharmaceutical Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Oxid Med Cell Longev</MedlineTA><NlmUniqueID>101479826</NlmUniqueID><ISSNLinking>1942-0994</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance UI="D008315">Malondialdehyde</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D031668" MajorTopicYN="N">Gastrodia</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="N">Glucosides</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008315" MajorTopicYN="N">Malondialdehyde</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050296" MajorTopicYN="N">Microbial Viability</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>05</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>05</Month><Day>29</Day></PubMedPubDate><PubMedPubDate 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name="République populaire de Chine"><region name="Zhejiang"><name sortKey="Lin, Yanfei" sort="Lin, Yanfei" uniqKey="Lin Y" first="Yanfei" last="Lin">Yanfei Lin</name></region><name sortKey="Qi, Jianhua" sort="Qi, Jianhua" uniqKey="Qi J" first="Jianhua" last="Qi">Jianhua Qi</name><name sortKey="Sun, Yujuan" sort="Sun, Yujuan" uniqKey="Sun Y" first="Yujuan" last="Sun">Yujuan Sun</name><name sortKey="Weng, Yufang" sort="Weng, Yufang" uniqKey="Weng Y" first="Yufang" last="Weng">Yufang Weng</name><name sortKey="Xiang, Lan" sort="Xiang, Lan" uniqKey="Xiang L" first="Lan" last="Xiang">Lan Xiang</name></country><country name="Japon"><noRegion><name sortKey="Matsuura, Akira" sort="Matsuura, Akira" uniqKey="Matsuura A" first="Akira" last="Matsuura">Akira Matsuura</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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