Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.
Identifieur interne : 000042 ( PubMed/Corpus ); précédent : 000041; suivant : 000043Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.
Auteurs : Jing-Ze Yu ; Yi Ying ; Yang Liu ; Chun-Bin Sun ; Chen Dai ; Shan Zhao ; Shou-Zheng Tian ; Jing Peng ; Ni-Ping Han ; Jia-Li Yuan ; Jin-Yuan Yan ; Zhong-Shan YangSource :
- Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [ 1950-6007 ] ; 2019.
English descriptors
- KwdEn :
- Animals, Autophagosomes (metabolism), Autophagosomes (ultrastructure), Autophagy (drug effects), Collagen (metabolism), Disease Models, Animal, Drugs, Chinese Herbal, Humans, Inflammation (complications), Inflammation (pathology), Lung (pathology), Male, Phosphatidylinositol 3-Kinases (metabolism), Phosphorylation (drug effects), Proto-Oncogene Proteins c-akt (metabolism), Pulmonary Fibrosis (complications), Pulmonary Fibrosis (drug therapy), Pulmonary Fibrosis (metabolism), Pulmonary Fibrosis (pathology), Signal Transduction, TOR Serine-Threonine Kinases (metabolism), Transforming Growth Factor beta1 (metabolism).
- MESH :
- chemical , metabolism : Collagen, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Transforming Growth Factor beta1.
- complications : Inflammation, Pulmonary Fibrosis.
- drug effects : Autophagy, Phosphorylation.
- drug therapy : Pulmonary Fibrosis.
- metabolism : Autophagosomes, Phosphatidylinositol 3-Kinases, Pulmonary Fibrosis.
- pathology : Inflammation, Lung, Pulmonary Fibrosis.
- ultrastructure : Autophagosomes.
- Animals, Disease Models, Animal, Drugs, Chinese Herbal, Humans, Male, Signal Transduction.
Abstract
Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is widely used for treatment of respiratory systems disease. However, the molecular basis for the function of YFSJF has not been determined. Here we investigate the contribution of YFSJF in BLM-induced PF mice. Administration with YFSJF significantly alleviated the degree of BLM-induced collagen I and III deposition and the inflammatory injuring in the lungs and suppressed hydroxyproline release in PF animals. The active components of YFSJF are comprised with flavonoid, amino acids, saponins, oligosaccharide, organic acid, vitamin, esters, purine nucleosides. Additionally, there was a significant increase in autophagosomes, after treatment with YFSJF in PF animals. Interestingly, autophagy dysfunction by the blocker chloroquine (CQ) resulted in collagen deposition and inducing the expression of fibrosis-related genes. In addition, YFSJF-induced autophagy is mediated by the PI3K-AKT-mTOR pathway, and knockdown of PI3K by siRNA up-regulated the expression of autophagy-related genes and down-regulated the expression of collagen in human lung fibroblasts (HLF). Our findings provide a detailed understanding that YFSJF-antifibrotic effects are mainly mediated by triggering autophagy, and suppressing phosphorylation of the PI3K-AKT-mTOR pathway is required for YFSJF-curative effect.
DOI: 10.1016/j.biopha.2019.109293
PubMed: 31401393
Links to Exploration step
pubmed:31401393Le document en format XML
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Electronic address: yangzhongshan@ynutcm.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31401393</idno><idno type="pmid">31401393</idno><idno type="doi">10.1016/j.biopha.2019.109293</idno><idno type="wicri:Area/PubMed/Corpus">000042</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000042</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.</title><author><name sortKey="Yu, Jing Ze" sort="Yu, Jing Ze" uniqKey="Yu J" first="Jing-Ze" last="Yu">Jing-Ze Yu</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ying, Yi" sort="Ying, Yi" uniqKey="Ying Y" first="Yi" last="Ying">Yi Ying</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Yang" sort="Liu, Yang" uniqKey="Liu Y" first="Yang" last="Liu">Yang Liu</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Sun, Chun Bin" sort="Sun, Chun Bin" uniqKey="Sun C" first="Chun-Bin" last="Sun">Chun-Bin Sun</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Dai, Chen" sort="Dai, Chen" uniqKey="Dai C" first="Chen" last="Dai">Chen Dai</name><affiliation><nlm:affiliation>Respiratory Department, Zhijiang Hospital of Chinese Medicine, Zhijiang, Hu Bei, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhao, Shan" sort="Zhao, Shan" uniqKey="Zhao S" first="Shan" last="Zhao">Shan Zhao</name><affiliation><nlm:affiliation>Rheumatology and Immunology Department, The First People's Hosipital of Yunnan Province, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Tian, Shou Zheng" sort="Tian, Shou Zheng" uniqKey="Tian S" first="Shou-Zheng" last="Tian">Shou-Zheng Tian</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Peng, Jing" sort="Peng, Jing" uniqKey="Peng J" first="Jing" last="Peng">Jing Peng</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Han, Ni Ping" sort="Han, Ni Ping" uniqKey="Han N" first="Ni-Ping" last="Han">Ni-Ping Han</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuan, Jia Li" sort="Yuan, Jia Li" uniqKey="Yuan J" first="Jia-Li" last="Yuan">Jia-Li Yuan</name><affiliation><nlm:affiliation>Yunnan Key Laboratory of Molecular Biology of Chinese Medicine, Kunming, Yunnan, China. Electronic address: 2748132800@qq.com.</nlm:affiliation></affiliation></author><author><name sortKey="Yan, Jin Yuan" sort="Yan, Jin Yuan" uniqKey="Yan J" first="Jin-Yuan" last="Yan">Jin-Yuan Yan</name><affiliation><nlm:affiliation>Central laboratory, The Second Affiliated Hospital of Kunming Medical Univ-ersity, Kunming, Yunnan, China. Electronic address: 399109308@qq.com.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Zhong Shan" sort="Yang, Zhong Shan" uniqKey="Yang Z" first="Zhong-Shan" last="Yang">Zhong-Shan Yang</name><affiliation><nlm:affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China. Electronic address: yangzhongshan@ynutcm.edu.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie</title><idno type="eISSN">1950-6007</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autophagosomes (metabolism)</term><term>Autophagosomes (ultrastructure)</term><term>Autophagy (drug effects)</term><term>Collagen (metabolism)</term><term>Disease Models, Animal</term><term>Drugs, Chinese Herbal</term><term>Humans</term><term>Inflammation (complications)</term><term>Inflammation (pathology)</term><term>Lung (pathology)</term><term>Male</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Phosphorylation (drug effects)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Pulmonary Fibrosis (complications)</term><term>Pulmonary Fibrosis (drug therapy)</term><term>Pulmonary Fibrosis (metabolism)</term><term>Pulmonary Fibrosis (pathology)</term><term>Signal Transduction</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Transforming Growth Factor beta1 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Collagen</term><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term><term>Transforming Growth Factor beta1</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Inflammation</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Phosphorylation</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term><term>Phosphatidylinositol 3-Kinases</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Lung</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Autophagosomes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drugs, Chinese Herbal</term><term>Humans</term><term>Male</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is widely used for treatment of respiratory systems disease. However, the molecular basis for the function of YFSJF has not been determined. Here we investigate the contribution of YFSJF in BLM-induced PF mice. Administration with YFSJF significantly alleviated the degree of BLM-induced collagen I and III deposition and the inflammatory injuring in the lungs and suppressed hydroxyproline release in PF animals. The active components of YFSJF are comprised with flavonoid, amino acids, saponins, oligosaccharide, organic acid, vitamin, esters, purine nucleosides. Additionally, there was a significant increase in autophagosomes, after treatment with YFSJF in PF animals. Interestingly, autophagy dysfunction by the blocker chloroquine (CQ) resulted in collagen deposition and inducing the expression of fibrosis-related genes. In addition, YFSJF-induced autophagy is mediated by the PI3K-AKT-mTOR pathway, and knockdown of PI3K by siRNA up-regulated the expression of autophagy-related genes and down-regulated the expression of collagen in human lung fibroblasts (HLF). Our findings provide a detailed understanding that YFSJF-antifibrotic effects are mainly mediated by triggering autophagy, and suppressing phosphorylation of the PI3K-AKT-mTOR pathway is required for YFSJF-curative effect.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31401393</PMID><DateCompleted><Year>2020</Year><Month>02</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1950-6007</ISSN><JournalIssue CitedMedium="Internet"><Volume>118</Volume><PubDate><Year>2019</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie</Title><ISOAbbreviation>Biomed. Pharmacother.</ISOAbbreviation></Journal><ArticleTitle>Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.</ArticleTitle><Pagination><MedlinePgn>109293</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0753-3322(19)32252-8</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biopha.2019.109293</ELocationID><Abstract><AbstractText>Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is widely used for treatment of respiratory systems disease. However, the molecular basis for the function of YFSJF has not been determined. Here we investigate the contribution of YFSJF in BLM-induced PF mice. Administration with YFSJF significantly alleviated the degree of BLM-induced collagen I and III deposition and the inflammatory injuring in the lungs and suppressed hydroxyproline release in PF animals. The active components of YFSJF are comprised with flavonoid, amino acids, saponins, oligosaccharide, organic acid, vitamin, esters, purine nucleosides. Additionally, there was a significant increase in autophagosomes, after treatment with YFSJF in PF animals. Interestingly, autophagy dysfunction by the blocker chloroquine (CQ) resulted in collagen deposition and inducing the expression of fibrosis-related genes. In addition, YFSJF-induced autophagy is mediated by the PI3K-AKT-mTOR pathway, and knockdown of PI3K by siRNA up-regulated the expression of autophagy-related genes and down-regulated the expression of collagen in human lung fibroblasts (HLF). Our findings provide a detailed understanding that YFSJF-antifibrotic effects are mainly mediated by triggering autophagy, and suppressing phosphorylation of the PI3K-AKT-mTOR pathway is required for YFSJF-curative effect.</AbstractText><CopyrightInformation>Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Jing-Ze</ForeName><Initials>JZ</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ying</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Chun-Bin</ForeName><Initials>CB</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Respiratory Department, Zhijiang Hospital of Chinese Medicine, Zhijiang, Hu Bei, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Shan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Rheumatology and Immunology Department, The First People's Hosipital of Yunnan Province, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tian</LastName><ForeName>Shou-Zheng</ForeName><Initials>SZ</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peng</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Ni-Ping</ForeName><Initials>NP</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Jia-Li</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Yunnan Key Laboratory of Molecular Biology of Chinese Medicine, Kunming, Yunnan, China. Electronic address: 2748132800@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Jin-Yuan</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Central laboratory, The Second Affiliated Hospital of Kunming Medical Univ-ersity, Kunming, Yunnan, China. Electronic address: 399109308@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Zhong-Shan</ForeName><Initials>ZS</Initials><AffiliationInfo><Affiliation>Faculty of Basic Medical Science, Yunnan Univer.0sity of Chinese Medicine, Kunming, Yunnan, China. Electronic address: yangzhongshan@ynutcm.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>08</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Biomed Pharmacother</MedlineTA><NlmUniqueID>8213295</NlmUniqueID><ISSNLinking>0753-3322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004365">Drugs, Chinese Herbal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053773">Transforming Growth Factor beta1</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-34-5</RegistryNumber><NameOfSubstance UI="D003094">Collagen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR 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MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004365" MajorTopicYN="N">Drugs, Chinese Herbal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011658" MajorTopicYN="N">Pulmonary Fibrosis</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" 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