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. 2015 Feb 16;13(2):1051-67.
doi: 10.3390/md13021051.

Fucoidan from Fucus vesiculosus protects against alcohol-induced liver damage by modulating inflammatory mediators in mice and HepG2 cells

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Fucoidan from Fucus vesiculosus protects against alcohol-induced liver damage by modulating inflammatory mediators in mice and HepG2 cells

Jung Dae Lim et al. Mar Drugs. .

Abstract

Fucoidan is an l-fucose-enriched sulfated polysaccharide isolated from brown algae and marine invertebrates. In this study, we investigated the protective effect of fucoidan from Fucus vesiculosus on alcohol-induced murine liver damage. Liver injury was induced by oral administration of 25% alcohol with or without fucoidan (30 mg/kg or 60 mg/kg) for seven days. Alcohol administration increased serum aspartate aminotransferase and alanine aminotransferase levels, but these increases were suppressed by the treatment of fucoidan. Transforming growth factor beta 1 (TGF-β1), a liver fibrosis-inducing factor, was highly expressed in the alcohol-fed group and human hepatoma HepG2 cell; however, the increase in TGF-β1 expression was reduced following fucoidan administration. Treatment with fucoidan was also found to significantly reduce the production of inflammation-promoting cyclooygenase-2 and nitric oxide, while markedly increasing the expression of the hepatoprotective enzyme, hemeoxygenase-1, on murine liver and HepG2 cells. Taken together, the antifibrotic and anti-inflammatory effects of fucoidan on alcohol-induced liver damage may provide valuable insights into developing new therapeutics or interventions.

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Figures

Figure 1
Figure 1
Experimental design.
Figure 2
Figure 2
Effect of fucoidan on alcohol-induced liver damage. (A) Serum aspartate aminotransferase (AST); (B) serum alanine aminotransferase (ALT). ## p < 0.01 vs. vehicle (n = 6); ** p < 0.01 vs. alcohol-fed group (n = 6).
Figure 3
Figure 3
Effect of fucoidan on alcohol-induced protein levels of transforming growth factor (TGF)-β1 in mice livers. (A) Representative immunoblot images of TGF-β1 and the loading control β-actin; (B) densitometry quantification of TGF-β1 expression normalized to β-actin. ## p < 0.05 vs. vehicle (n = 6); ** p < 0.5 vs. alcohol-fed group (n = 6).
Figure 4
Figure 4
Effect of fucoidan on alcohol-induced protein levels of TGF-β1 in HepG2 cells. (A) Representative immunoblot images of TGF-β1 and the loading control β-actin; (B) densitometry quantification of TGF-β1 expression normalized to β-actin. ## p < 0.05 vs. vehicle (n = 6); ** p < 0.5 vs. alcohol-treated group (n = 6).
Figure 5
Figure 5
Effect of fucoidan on nitric oxide production and protein expression levels of inducible nitric oxide synthase (iNOS) following alcohol exposure. (A) Nitric oxide (NO) production in HepG2 cells. Representative immunoblots and densitometry quantification of iNOS expression in HepG2 (B) and murine liver (C), both normalized to β-actin expression. # p < 0.05 vs. vehicle (n = 6); * p < 0.05 vs. alcohol-treated group (n = 6).
Figure 6
Figure 6
Effect of fucoidan on alcohol-induced expression levels of cyclooxygenase (COX)-2 in murine liver. (A) Representative immunoblot images of COX-2 and β-actin; (B) quantification of COX-2 expression normalized to β-actin. ## p < 0.01 vs. vehicle (n = 6); ** p < 0.01 vs. alcohol-fed group (n = 6).
Figure 7
Figure 7
Effect of fucoidan on alcohol-induced expression levels of COX-2 in HepG2 cells. (A) Representative immunoblot images of COX-2 and the loading control β-actin; (B) quantification of COX-2 expression normalized to β-actin. ## p < 0.01 vs. vehicle (n = 6); * p < 0.05 and ** p < 0.01 vs. alcohol-treated group (n = 6).
Figure 8
Figure 8
Effect of fucoidan on alcohol-induced expression levels of heme oxygenase (HO)-1 in murine liver. (A) Representative immunoblot images of HO-1 and the loading control β-actin; (B) quantification of HO-1 expression normalized to β-actin. ## p < 0.05 vs. vehicle (n = 6).
Figure 9
Figure 9
Effect of fucoidan on alcohol-induced expression levels of HO-1 in HepG2 cells. (A) Representative immunoblot images of HO-1 and β-actin; (B) quantification of HO-1 expression normalized to β-actin. ## p < 0.05 vs. vehicle (n = 6).

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