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Inhibitory Effect of Fucoidan on TGF-β1-Induced Activation of Human Pulmonary Fibroblasts

후코이단에 의한 인간 폐 섬유모세포의 활성 억제 효과

  • Yim, Mi-Jin (Natural Products Research Team, National Marine Biodiversity Institute of Korea) ;
  • Lee, Dae-Sung (Natural Products Research Team, National Marine Biodiversity Institute of Korea) ;
  • Choi, Grace (Natural Products Research Team, National Marine Biodiversity Institute of Korea) ;
  • Lee, Jeong Min (Natural Products Research Team, National Marine Biodiversity Institute of Korea) ;
  • Choi, Il-Whan (Department of Microbiology and Immunology, College of Medicine Inje University)
  • 임미진 (국립해양생물자원관 천연물연구팀) ;
  • 이대성 (국립해양생물자원관 천연물연구팀) ;
  • 최그레이스 (국립해양생물자원관 천연물연구팀) ;
  • 이정민 (국립해양생물자원관 천연물연구팀) ;
  • 최일환 (인제대학교 의과대학 미생물학교실)
  • Received : 2016.10.06
  • Accepted : 2016.11.07
  • Published : 2016.12.31

Abstract

Fucoidan, one of the dominant sulfated polysaccharides extracted from brown seaweed, possesses a wide range of biological activities. Transforming growth $factor-{\beta}$ ($TGF-{\beta}$) plays a pivotal role in the pathogenesis of pulmonary fibrosis, by stimulating the synthesis of profibrotic factors. In this study, we investigated the in vitro effects of fucoidan on collagen synthesis, ${\alpha}-smooth$ muscle actin (${\alpha}-SMA$) expression, and interleukin (IL)-6 production in $TGF-{\beta}$-stimulated human pulmonary fibroblasts. The expression of type I collagen and ${\alpha}-SMA$ was detected by Western blot, and the production of IL-6 by enzyme-linked immunosorbent assay. $TGF-{\beta}1$ treatment of pulmonary fibroblasts enhanced the expression of ${\alpha}-SMA$, type I collagen, and IL-6 whereas these effects were inhibited in cells pretreated with fucoidan. The activation of Smad2/3, p38 mitogen-activated protein kinases (MAPKs), and Akt was also inhibited in fucoidan-pretreated, $TGF-{\beta}1-stimulated$ human pulmonary fibroblasts. These data demonstrate the anti-fibrotic potential of fucoidan in $TGF-{\beta}-induced$ human pulmonary fibroblasts, via the inhibition of Smad2/3, p38 MAPKs, and Akt phosphorylation. Our results suggest the therapeutic potential of fucoidan in the prevention or treatment of pulmonary fibrosis.

Keywords

References

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