Effects of scutellarin on MUC5AC mucin production induced by human neutrophil elastase or interleukin 13 on airway epithelial cells

J Korean Med Sci. 2011 Jun;26(6):778-84. doi: 10.3346/jkms.2011.26.6.778. Epub 2011 May 18.

Abstract

Scutellarin is a flavonoid extracted from a traditional Chinese herb, Erigeron breviscapus. The present study investigated the effect of scutellarin on MUC5AC mucin production and the possible mechanism. Human bronchial epithelial 16 (HBE16) cells were pretreated with scutellarin for 60 min, and then exposed to human neutrophil elastase (HNE) or interleukin (IL)-13 for 12 hr. RT-PCR and ELISA were performed to measure the amount of MUC5AC mucin production. The results showed that scutellarin inhibited MUC5AC expression both in mRNA and protein level induced by HNE in a concentration-dependent manner. However, scutellarin failed to inhibit MUC5AC mucin production induced by IL-13. To investigate the intracellular mechanisms associated with the effect of scutellarin on MUC5AC mucin production, western blotting was carried out to examine the phosphorylation of protein kinase C (PKC), signal transducer and activator of transcription 6 (STAT6) and extracellular signal-regulated kinase 1/2 (ERK1/2). The phosphorylation of PKC and ERK1/2 was attenuated after treatment with scutellarin, whereas STAT6 was not significantly affected. Therefore, it is suggested that scutellarin down-regulates MUC5AC mucin production on HBE16 cells via ERK-dependent and PKC-dependent pathways.

Keywords: Airway Epithelial Cells; Human Neutrophil Elastase; Interleukin-13; MUC5AC; Scutellarin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apigenin / chemistry
  • Apigenin / pharmacology*
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Down-Regulation
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Erigeron / chemistry
  • Glucuronates / chemistry
  • Glucuronates / pharmacology*
  • Humans
  • Interleukin-13 / pharmacology*
  • Leukocyte Elastase / pharmacology*
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Mucin 5AC / genetics
  • Mucin 5AC / metabolism*
  • Phosphorylation
  • Protein Kinase C / metabolism
  • Respiratory Mucosa / drug effects
  • Respiratory Mucosa / metabolism*
  • STAT6 Transcription Factor / metabolism
  • Signal Transduction

Substances

  • Glucuronates
  • Interleukin-13
  • Mucin 5AC
  • STAT6 Transcription Factor
  • scutellarin
  • Apigenin
  • Protein Kinase C
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Leukocyte Elastase