Casticin alleviates lipopolysaccharide‐induced inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells through Nrf2/Keap1 and NF‐κB pathways

Asthma is one of the most common chronic inflammatory diseases of childhood, characterized by airway inflammation, mucus hypersecretion, and accumulation of extracellular matrix proteins. Casticin is an active compound that possesses broad biological activities including anti‐inflammatory effect. Ho...

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Bibliographic Details
Published in:Phytotherapy research 2018-07, Vol.32 (7), p.1346-1353
Main Author: Wang, Jiusheng
Format: Article
Language:English
Subjects:
Asthma
casticin
Children
Collagen
Collagen (type I)
Epithelial cells
Extracellular matrix
Fibronectin
inflammation
Inflammatory diseases
Lipopolysaccharides
mRNA
Mucous membrane
Mucus
Proteins
Respiratory tract
Respiratory tract diseases
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Summary:Asthma is one of the most common chronic inflammatory diseases of childhood, characterized by airway inflammation, mucus hypersecretion, and accumulation of extracellular matrix proteins. Casticin is an active compound that possesses broad biological activities including anti‐inflammatory effect. However, the effect of casticin on asthma remains unknown. The aim of the present study was to evaluate the effect and mechanism of casticin on inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells. The results showed that lipopolysaccharide induced the mRNA and protein levels of IL‐6, IL‐8, MUC5AC, collagen type I, and fibronectin in 16‐HBE cells, whereas casticin treatment significantly inhibited the induction of lipopolysaccharide. Casticin induced Nrf2/Keap1 and inhibited nuclear factor κB pathways in 16‐HBE cells. Knockdown of Nrf2 attenuated the effect of casticin on production of IL‐6 and IL‐8, expression of MUC5AC, collagen type I, and fibronectin in 16‐HBE cells. In conclusion, the results indicated that casticin might be a novel therapeutic strategy for the treatment of asthma.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.6067