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:
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Le document en format XML
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<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>
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<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>
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