후코이단에 의한 인간 폐 섬유모세포의 활성 억제 효과 (Inhibitory Effect of Fucoidan on TGF-β1-Induced Activation of Human Pulmonary Fibroblasts)

서지정보

· 발행기관 : 한국수산과학회
· 수록지 정보 : 한국수산과학회지 / 49권 / 6호 / 807 ~ 814페이지
· 저자명 : 임미진, 이대성, 최그레이스, 이정민, 최일환

초록

Fucoidan, one of the dominant sulfated polysaccharides extracted from brown seaweed, possesses a wide range of biological activities. Transforming growth factor-β (TGF-β) 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, α-smooth muscle actin (α-SMA) expression, and interleukin (IL)-6 production in TGF-β-stimulated human pulmonary fibroblasts. The expression of type I collagen and α-SMA was detected by Western blot, and the production of IL-6 by enzyme-linked immunosorbent assay. TGF-β1 treatment of pulmonary fibroblasts enhanced the expression of α-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-β1-stimulated human pulmonary fibroblasts. These data demonstrate the anti-fibrotic potential of fucoidan in TGF-β-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.

영어초록

Fucoidan, one of the dominant sulfated polysaccharides extracted from brown seaweed, possesses a wide range of biological activities. Transforming growth factor-β (TGF-β) 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, α-smooth muscle actin (α-SMA) expression, and interleukin (IL)-6 production in TGF-β-stimulated human pulmonary fibroblasts. The expression of type I collagen and α-SMA was detected by Western blot, and the production of IL-6 by enzyme-linked immunosorbent assay. TGF-β1 treatment of pulmonary fibroblasts enhanced the expression of α-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-β1-stimulated human pulmonary fibroblasts. These data demonstrate the anti-fibrotic potential of fucoidan in TGF-β-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.

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