Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.
Identifieur interne : 000032 ( PubMed/Curation ); précédent : 000031; suivant : 000033Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.
Auteurs : Hangqi Liu [République populaire de Chine] ; He Yu [République populaire de Chine] ; Zhenju Cao [République populaire de Chine] ; Junxu Gu [République populaire de Chine] ; Lin Pei [République populaire de Chine] ; Mei Jia [République populaire de Chine] ; Ming Su [République populaire de Chine]Source :
- DNA and cell biology [ 1557-7430 ] ; 2019.
Descripteurs français
- KwdFr :
- MESH :
- effets indésirables : Silice.
- pharmacologie : Kaempférols.
- étiologie : Silicose.
- Animaux, Autophagie, Fibrose pulmonaire, Modèles animaux de maladie humaine, Mâle, Silicose, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- MESH :
- chemical , adverse effects : Silicon Dioxide.
- chemical , pharmacology : Kaempferols.
- chemically induced : Pulmonary Fibrosis.
- etiology : Silicosis.
- prevention & control : Pulmonary Fibrosis, Silicosis.
- Animals, Autophagy, Disease Models, Animal, Male, Mice, Mice, Inbred C57BL.
Abstract
Silicosis is an occupational disease characterized as inflammatory cells infiltration and severe progressive pulmonary fibrosis. Kaempferol (Kae), a flavonoid that exists in many plants and fruits, has been proved to have anti-inflammatory and antifibrosis functions. However, the effects of Kae on silicosis remain unclear. In the present study, we analyzed the therapeutic effects of Kae in 1-, 7-, and 28-day silicosis models, respectively. In the 1-day model, Kae treatment did not vary the wet-to-dry weight ratios of the lung, apoptotic rate, autophagy, or the expression of inflammatory factors. In contrast, Kae significantly inhibited pulmonary inflammation in the 7-day silicosis models and inhibited silica-induced pulmonary fibrosis in the 28-day models. Besides, we found that Kae partially restored silica-induced LC3 lipidation without increasing the p62 levels. Blocking autophagy with chloroquine antagonized the inhibitory effects of Kae on inflammation, suggesting that autophagy might be required in the therapeutic effects of Kae on silicosis. These findings indicated that Kae inhibits the progression of silica-induced pulmonary fibrosis, which may provide experimental evidences for Kae in the treatment of silicosis.
DOI: 10.1089/dna.2019.4941
PubMed: 31560574
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(prevention & control)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Fibrose pulmonaire ()</term><term>Kaempférols (pharmacologie)</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Silice (effets indésirables)</term><term>Silicose ()</term><term>Silicose (étiologie)</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Silicon Dioxide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Kaempferols</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Silice</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Silicosis</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Kaempférols</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Pulmonary Fibrosis</term><term>Silicosis</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Silicose</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Disease Models, Animal</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Fibrose pulmonaire</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Silicose</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Silicosis is an occupational disease characterized as inflammatory cells infiltration and severe progressive pulmonary fibrosis. Kaempferol (Kae), a flavonoid that exists in many plants and fruits, has been proved to have anti-inflammatory and antifibrosis functions. However, the effects of Kae on silicosis remain unclear. In the present study, we analyzed the therapeutic effects of Kae in 1-, 7-, and 28-day silicosis models, respectively. In the 1-day model, Kae treatment did not vary the wet-to-dry weight ratios of the lung, apoptotic rate, autophagy, or the expression of inflammatory factors. In contrast, Kae significantly inhibited pulmonary inflammation in the 7-day silicosis models and inhibited silica-induced pulmonary fibrosis in the 28-day models. Besides, we found that Kae partially restored silica-induced LC3 lipidation without increasing the p62 levels. Blocking autophagy with chloroquine antagonized the inhibitory effects of Kae on inflammation, suggesting that autophagy might be required in the therapeutic effects of Kae on silicosis. These findings indicated that Kae inhibits the progression of silica-induced pulmonary fibrosis, which may provide experimental evidences for Kae in the treatment of silicosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31560574</PMID><DateCompleted><Year>2019</Year><Month>12</Month><Day>27</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7430</ISSN><JournalIssue CitedMedium="Internet"><Volume>38</Volume><Issue>12</Issue><PubDate><Year>2019</Year><Month>Dec</Month></PubDate></JournalIssue><Title>DNA and cell biology</Title><ISOAbbreviation>DNA Cell Biol.</ISOAbbreviation></Journal><ArticleTitle>Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.</ArticleTitle><Pagination><MedlinePgn>1418-1426</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1089/dna.2019.4941</ELocationID><Abstract><AbstractText>Silicosis is an occupational disease characterized as inflammatory cells infiltration and severe progressive pulmonary fibrosis. Kaempferol (Kae), a flavonoid that exists in many plants and fruits, has been proved to have anti-inflammatory and antifibrosis functions. However, the effects of Kae on silicosis remain unclear. In the present study, we analyzed the therapeutic effects of Kae in 1-, 7-, and 28-day silicosis models, respectively. In the 1-day model, Kae treatment did not vary the wet-to-dry weight ratios of the lung, apoptotic rate, autophagy, or the expression of inflammatory factors. In contrast, Kae significantly inhibited pulmonary inflammation in the 7-day silicosis models and inhibited silica-induced pulmonary fibrosis in the 28-day models. Besides, we found that Kae partially restored silica-induced LC3 lipidation without increasing the p62 levels. Blocking autophagy with chloroquine antagonized the inhibitory effects of Kae on inflammation, suggesting that autophagy might be required in the therapeutic effects of Kae on silicosis. These findings indicated that Kae inhibits the progression of silica-induced pulmonary fibrosis, which may provide experimental evidences for Kae in the treatment of silicosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Hangqi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>He</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Zhenju</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Junxu</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pei</LastName><ForeName>Lin</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Mei</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Ming</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>09</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>DNA Cell Biol</MedlineTA><NlmUniqueID>9004522</NlmUniqueID><ISSNLinking>1044-5498</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D044949">Kaempferols</NameOfSubstance></Chemical><Chemical><RegistryNumber>731P2LE49E</RegistryNumber><NameOfSubstance UI="C006552">kaempferol</NameOfSubstance></Chemical><Chemical><RegistryNumber>7631-86-9</RegistryNumber><NameOfSubstance UI="D012822">Silicon Dioxide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044949" MajorTopicYN="N">Kaempferols</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011658" MajorTopicYN="N">Pulmonary Fibrosis</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012822" MajorTopicYN="N">Silicon Dioxide</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012829" MajorTopicYN="N">Silicosis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">kaempferol</Keyword><Keyword MajorTopicYN="N">silicosis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>12</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>9</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31560574</ArticleId><ArticleId IdType="doi">10.1089/dna.2019.4941</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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