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

Ji Won Park, Na Rae Shin, In Sik Shin, Ok Kyoung Kwon, Joong Sun Kim, Sei Ryang Oh, Jae-Hong Kim, Kyung Seop Ahn

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1926-1936
Number of pages11
JournalPhytotherapy Research
Volume30
Issue number12
DOIs
Publication statusPublished - 2016 Dec 1

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Extracellular Signal-Regulated MAP Kinases
Mucus
Smoke
Tobacco Products
Inflammation
Chronic Obstructive Pulmonary Disease
Lipopolysaccharides
Phosphorylation
silybin
Silymarin
Peroxidase
Liver Diseases
Anti-Inflammatory Agents
Down-Regulation

Keywords

  • chronic obstructive pulmonary disease
  • cigarette smoke
  • silibinin (PubChem CID: 31553)
  • SP-1

ASJC Scopus subject areas

  • Pharmacology

Cite this

Park, J. W., Shin, N. R., Shin, I. S., Kwon, O. K., Kim, J. S., Oh, S. R., ... Ahn, K. S. (2016). Silibinin Inhibits Neutrophilic Inflammation and Mucus Secretion Induced by Cigarette Smoke via Suppression of ERK-SP1 Pathway. Phytotherapy Research, 30(12), 1926-1936. https://doi.org/10.1002/ptr.5686

Silibinin Inhibits Neutrophilic Inflammation and Mucus Secretion Induced by Cigarette Smoke via Suppression of ERK-SP1 Pathway. / Park, Ji Won; Shin, Na Rae; Shin, In Sik; Kwon, Ok Kyoung; Kim, Joong Sun; Oh, Sei Ryang; Kim, Jae-Hong; Ahn, Kyung Seop.

In: Phytotherapy Research, Vol. 30, No. 12, 01.12.2016, p. 1926-1936.

Research output: Contribution to journalArticle

Park, Ji Won ; Shin, Na Rae ; Shin, In Sik ; Kwon, Ok Kyoung ; Kim, Joong Sun ; Oh, Sei Ryang ; Kim, Jae-Hong ; Ahn, Kyung Seop. / Silibinin Inhibits Neutrophilic Inflammation and Mucus Secretion Induced by Cigarette Smoke via Suppression of ERK-SP1 Pathway. In: Phytotherapy Research. 2016 ; Vol. 30, No. 12. pp. 1926-1936.
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