Silibinin Inhibits Neutrophilic Inflammation and Mucus Secretion Induced by Cigarette Smoke via Suppression of ERK-SP1 Pathway

Silibinin, the main ingredient of silymarin, has been used as a traditional drug for over 2000 years to treat a range of liver diseases. Recent studies have also demonstrated that silibinin possesses antiinflammatory and anticancer properties. In the study, we researched the efficacy of silibinin on...

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Published in:Phytotherapy research 2016-12, Vol.30 (12), p.1926-1936
Main Authors: Park, Ji-Won, Shin, Na-Rae, Shin, In-Sik, Kwon, Ok-Kyoung, Kim, Joong-Sun, Oh, Sei-Ryang, Kim, Jae-hong, Ahn, Kyung-Seop
Format: Article
Language:English
Subjects:
Animals
chronic obstructive pulmonary disease
cigarette smoke
Extracellular Signal-Regulated MAP Kinases - metabolism
Inflammation - metabolism
Male
Mice
Mice, Inbred C57BL
Mucus - secretion
Neutrophils - metabolism
Phosphorylation
Plants, Medicinal - chemistry
Reactive Oxygen Species
Signal Transduction
silibinin (PubChem CID: 31553)
Silymarin - metabolism
SP-1
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Summary:Silibinin, the main ingredient of silymarin, has been used as a traditional drug for over 2000 years to treat a range of liver diseases. Recent studies have also demonstrated that silibinin possesses antiinflammatory and anticancer properties. In the study, we researched the efficacy of silibinin on the development of COPD using a cigarette smoke (CS)‐induced and lipopolysaccharide (LPS)‐induced COPD model mice and stimulation of NCI‐H292 cells with CS condensate. Silibinin was administered to mice by oral gavage 1 h before CS exposure for 10 days. In in vitro experiment, we evaluated the effect of silibinin on the expression of MUC5AC in H292 cells stimulated with CS condensate. Furthermore, silibinin suppressed the CS and LPS treatment‐induced extracellular signal‐regulated kinase (ERK) phosphorylation and SP‐1 expression. Silibinin also decreased airway inflammation and reduced the expression of MUC5AC and myeloperoxidase. Furthermore, co‐treatment with silibinin and ERK inhibitors considerably decreased the levels of pro‐inflammatory mediators, ERK phosphorylation, and SP‐1 expression. Taken together, the results indicate that silibinin effectively suppressed the neutrophilic airway inflammation provoked by treatment with LPS and CS, which was closely associated with downregulation of ERK phosphorylation. Therefore, our searching offers that silibinin has a remedical probable for COPD disease. Copyright © 2016 John Wiley & Sons, Ltd.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.5686