Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.
Identifieur interne : 000705 ( Main/Exploration ); précédent : 000704; suivant : 000706Kaempferol 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
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000032
- to stream PubMed, to step Curation: 000032
- to stream PubMed, to step Checkpoint: 000044
- to stream Ncbi, to step Merge: 000A62
- to stream Ncbi, to step Curation: 000A62
- to stream Ncbi, to step Checkpoint: 000A62
- to stream Main, to step Merge: 000705
- to stream Main, to step Curation: 000705
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.</title><author><name sortKey="Liu, Hangqi" sort="Liu, Hangqi" uniqKey="Liu H" first="Hangqi" last="Liu">Hangqi Liu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Yu, He" sort="Yu, He" uniqKey="Yu H" first="He" last="Yu">He Yu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Cao, Zhenju" sort="Cao, Zhenju" uniqKey="Cao Z" first="Zhenju" last="Cao">Zhenju Cao</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Gu, Junxu" sort="Gu, Junxu" uniqKey="Gu J" first="Junxu" last="Gu">Junxu Gu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Pei, Lin" sort="Pei, Lin" uniqKey="Pei L" first="Lin" last="Pei">Lin Pei</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Jia, Mei" sort="Jia, Mei" uniqKey="Jia M" first="Mei" last="Jia">Mei Jia</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Su, Ming" sort="Su, Ming" uniqKey="Su M" first="Ming" last="Su">Ming Su</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31560574</idno><idno type="pmid">31560574</idno><idno type="doi">10.1089/dna.2019.4941</idno><idno type="wicri:Area/PubMed/Corpus">000032</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000032</idno><idno type="wicri:Area/PubMed/Curation">000032</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000032</idno><idno type="wicri:Area/PubMed/Checkpoint">000044</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000044</idno><idno type="wicri:Area/Ncbi/Merge">000A62</idno><idno type="wicri:Area/Ncbi/Curation">000A62</idno><idno type="wicri:Area/Ncbi/Checkpoint">000A62</idno><idno type="wicri:Area/Main/Merge">000705</idno><idno type="wicri:Area/Main/Curation">000705</idno><idno type="wicri:Area/Main/Exploration">000705</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.</title><author><name sortKey="Liu, Hangqi" sort="Liu, Hangqi" uniqKey="Liu H" first="Hangqi" last="Liu">Hangqi Liu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Yu, He" sort="Yu, He" uniqKey="Yu H" first="He" last="Yu">He Yu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Cao, Zhenju" sort="Cao, Zhenju" uniqKey="Cao Z" first="Zhenju" last="Cao">Zhenju Cao</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Gu, Junxu" sort="Gu, Junxu" uniqKey="Gu J" first="Junxu" last="Gu">Junxu Gu</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Pei, Lin" sort="Pei, Lin" uniqKey="Pei L" first="Lin" last="Pei">Lin Pei</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Jia, Mei" sort="Jia, Mei" uniqKey="Jia M" first="Mei" last="Jia">Mei Jia</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Su, Ming" sort="Su, Ming" uniqKey="Su M" first="Ming" last="Su">Ming Su</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">DNA and cell biology</title><idno type="eISSN">1557-7430</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>Autophagy</term><term>Disease Models, Animal</term><term>Kaempferols (pharmacology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Pulmonary Fibrosis (chemically induced)</term><term>Pulmonary Fibrosis (prevention & control)</term><term>Silicon Dioxide (adverse effects)</term><term>Silicosis (etiology)</term><term>Silicosis (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><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Liu, Hangqi" sort="Liu, Hangqi" uniqKey="Liu H" first="Hangqi" last="Liu">Hangqi Liu</name></noRegion><name sortKey="Cao, Zhenju" sort="Cao, Zhenju" uniqKey="Cao Z" first="Zhenju" last="Cao">Zhenju Cao</name><name sortKey="Gu, Junxu" sort="Gu, Junxu" uniqKey="Gu J" first="Junxu" last="Gu">Junxu Gu</name><name sortKey="Jia, Mei" sort="Jia, Mei" uniqKey="Jia M" first="Mei" last="Jia">Mei Jia</name><name sortKey="Pei, Lin" sort="Pei, Lin" uniqKey="Pei L" first="Lin" last="Pei">Lin Pei</name><name sortKey="Su, Ming" sort="Su, Ming" uniqKey="Su M" first="Ming" last="Su">Ming Su</name><name sortKey="Yu, He" sort="Yu, He" uniqKey="Yu H" first="He" last="Yu">He Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000705 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000705 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:31560574
|texte= Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:31560574" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |