Inhibitory effect of delphinidin on extracellular matrix production via the MAPK/NF-κB pathway in nasal polyp-derived fibroblasts

Jung Sun Cho, Ju Hyung Kang, Jae Min Shin, Il Ho Park, Heung Man Lee

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Purpose: Nasal polyps are associated with chronic inflammation of the mucous membranes in the nose and paranasal sinuses and involved in extracellular matrix (ECM) accumulation. Delphinidin promotes ECM degradation in hepatitis and cardiac fibrosis. The aims of this study were to examine the inhibitory effect of delphinidin on TGF-β1-induced myofibroblast differentiation and ECM accumulation, and to determine the underlying mechanisms in nasal polyp-derived fibroblasts (NPDFs). Methods: NPDFs were stimulated with TGF-β1, with or without delphinidin, and the expression levels of α-SMA, fibronectin, and collagen type I were determined by RT-PCR, Western blot analysis, and collagen assay. The expression of α-SMA protein was measured by immunocytochemical staining. Mitogen-activated protein kinase and NF-κB activation induced by TGF-β1 were determined by Western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay. Results: The expression levels of α-SMA, fibronectin, and collagen type I increased in TGF-β1-stimulated NPDFs. In TGF-β1-induced NPDFs, delphinidin inhibited the expression of α-SMA, fibronectin, and collagen. Inhibitors of MAPK and NF-κB blocked the expression of α-SMA, fibronectin, and collagen type I. Delphinidin suppressed the activation of MAPK and NF-κB induced by TGF-β1 stimulation. Conclusions: These results suggest that delphinidin may inhibit TGF- β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.

Original languageEnglish
Pages (from-to)276-282
Number of pages7
JournalAllergy, Asthma and Immunology Research
Volume7
Issue number3
DOIs
Publication statusPublished - 2015

Fingerprint

delphinidin
Nasal Polyps
Extracellular Matrix
Fibroblasts
Fibronectins
Collagen Type I
Myofibroblasts
Collagen
Western Blotting
Proto-Oncogene Proteins c-akt
Paranasal Sinuses
Mitogen-Activated Protein Kinases
Luciferases
Nose
Hepatitis
Mucous Membrane
Fibrosis

Keywords

  • Chronic rhinosinusitis
  • Delphinidin
  • Extracellular matrix
  • MAPK
  • Myofibroblast
  • Nasal polyposis
  • NF-κB
  • TGF-β1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pulmonary and Respiratory Medicine

Cite this

Inhibitory effect of delphinidin on extracellular matrix production via the MAPK/NF-κB pathway in nasal polyp-derived fibroblasts. / Cho, Jung Sun; Kang, Ju Hyung; Shin, Jae Min; Park, Il Ho; Lee, Heung Man.

In: Allergy, Asthma and Immunology Research, Vol. 7, No. 3, 2015, p. 276-282.

Research output: Contribution to journalArticle

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abstract = "Purpose: Nasal polyps are associated with chronic inflammation of the mucous membranes in the nose and paranasal sinuses and involved in extracellular matrix (ECM) accumulation. Delphinidin promotes ECM degradation in hepatitis and cardiac fibrosis. The aims of this study were to examine the inhibitory effect of delphinidin on TGF-β1-induced myofibroblast differentiation and ECM accumulation, and to determine the underlying mechanisms in nasal polyp-derived fibroblasts (NPDFs). Methods: NPDFs were stimulated with TGF-β1, with or without delphinidin, and the expression levels of α-SMA, fibronectin, and collagen type I were determined by RT-PCR, Western blot analysis, and collagen assay. The expression of α-SMA protein was measured by immunocytochemical staining. Mitogen-activated protein kinase and NF-κB activation induced by TGF-β1 were determined by Western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay. Results: The expression levels of α-SMA, fibronectin, and collagen type I increased in TGF-β1-stimulated NPDFs. In TGF-β1-induced NPDFs, delphinidin inhibited the expression of α-SMA, fibronectin, and collagen. Inhibitors of MAPK and NF-κB blocked the expression of α-SMA, fibronectin, and collagen type I. Delphinidin suppressed the activation of MAPK and NF-κB induced by TGF-β1 stimulation. Conclusions: These results suggest that delphinidin may inhibit TGF- β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.",
keywords = "Chronic rhinosinusitis, Delphinidin, Extracellular matrix, MAPK, Myofibroblast, Nasal polyposis, NF-κB, TGF-β1",
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AU - Kang, Ju Hyung

AU - Shin, Jae Min

AU - Park, Il Ho

AU - Lee, Heung Man

PY - 2015

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N2 - Purpose: Nasal polyps are associated with chronic inflammation of the mucous membranes in the nose and paranasal sinuses and involved in extracellular matrix (ECM) accumulation. Delphinidin promotes ECM degradation in hepatitis and cardiac fibrosis. The aims of this study were to examine the inhibitory effect of delphinidin on TGF-β1-induced myofibroblast differentiation and ECM accumulation, and to determine the underlying mechanisms in nasal polyp-derived fibroblasts (NPDFs). Methods: NPDFs were stimulated with TGF-β1, with or without delphinidin, and the expression levels of α-SMA, fibronectin, and collagen type I were determined by RT-PCR, Western blot analysis, and collagen assay. The expression of α-SMA protein was measured by immunocytochemical staining. Mitogen-activated protein kinase and NF-κB activation induced by TGF-β1 were determined by Western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay. Results: The expression levels of α-SMA, fibronectin, and collagen type I increased in TGF-β1-stimulated NPDFs. In TGF-β1-induced NPDFs, delphinidin inhibited the expression of α-SMA, fibronectin, and collagen. Inhibitors of MAPK and NF-κB blocked the expression of α-SMA, fibronectin, and collagen type I. Delphinidin suppressed the activation of MAPK and NF-κB induced by TGF-β1 stimulation. Conclusions: These results suggest that delphinidin may inhibit TGF- β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.

AB - Purpose: Nasal polyps are associated with chronic inflammation of the mucous membranes in the nose and paranasal sinuses and involved in extracellular matrix (ECM) accumulation. Delphinidin promotes ECM degradation in hepatitis and cardiac fibrosis. The aims of this study were to examine the inhibitory effect of delphinidin on TGF-β1-induced myofibroblast differentiation and ECM accumulation, and to determine the underlying mechanisms in nasal polyp-derived fibroblasts (NPDFs). Methods: NPDFs were stimulated with TGF-β1, with or without delphinidin, and the expression levels of α-SMA, fibronectin, and collagen type I were determined by RT-PCR, Western blot analysis, and collagen assay. The expression of α-SMA protein was measured by immunocytochemical staining. Mitogen-activated protein kinase and NF-κB activation induced by TGF-β1 were determined by Western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay. Results: The expression levels of α-SMA, fibronectin, and collagen type I increased in TGF-β1-stimulated NPDFs. In TGF-β1-induced NPDFs, delphinidin inhibited the expression of α-SMA, fibronectin, and collagen. Inhibitors of MAPK and NF-κB blocked the expression of α-SMA, fibronectin, and collagen type I. Delphinidin suppressed the activation of MAPK and NF-κB induced by TGF-β1 stimulation. Conclusions: These results suggest that delphinidin may inhibit TGF- β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.

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KW - Nasal polyposis

KW - NF-κB

KW - TGF-β1

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