• KSBB Journal
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• v.22 no.4
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• pp.265-269
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• 2007

Fucoidan from sea tangle (Laminaria japonica) was isolated by hot water extraction, and partially purified. The in-vitro glucose and bile acid retarding effects of the partially purified fucoidan were investigated. Fucoidan exhibited 27.06$\sim$21.42% of retarding index for glucose and 33.50$\sim$27.02% of retarding index for bile acid during in vitro dialysis experiment for 2 hours. These retarding effects on glucose and bile acid diffusion was considered as a relatively good or very good, suggesting the prevention from diabetes and arteriosclerosis of some extent.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.4
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• pp.327-331
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• 2014

In this study we investigated the effects of fucoidan on the proliferation of fibroblasts and the reconstruction of a skin equivalent (SE). Fucoidan significantly stimulated the proliferation of CCD-25Sk human fibroblasts and Western blot analysis demonstrated that fucoidan markedly increased the expression of cyclin D1 and decreased the expression of p27. Fucoidan was used to reconstruct SE. Immunohistochemical staining showed that the addition of fucoidan to dermal equivalents increased expression of proliferating cell nuclear antigen (PCNA) and p63. In addition, expression of ${\alpha}6$-integrin was significantly increased by fucoidan, whereas expression of ${\beta}1$-integrin, type 1 collagen, elastin, fibronectin did not markedly change. These results suggest that fucoidan has positive effects on epidermal reconstruction and will therefore be beneficial in the reconstruction of SE.

• Nutrition Research and Practice
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• v.17 no.5
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• pp.844-854
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• 2023

BACKGROUND/OBJECTIVES: Fucoidan, a polysaccharide content in brown algae, has been reported to inhibit the growth of cancer cells. The present study aimed to investigate the suppression effects of fucoidan on A549 non-small cell lung cancer cells migration. MATERIALS/METHODS: The anti-migratory activity of fucoidan in A549 cells was examined by wound healing assay and phalloidin-rhodamine staining in response to fucoidan (0-100 ㎍/mL) treatment for 48 h. Western blot analysis was performed to clarify the protein expressions relevant to migratory activity. RESULTS: Fucoidan (25-100 ㎍/mL) significantly suppressed A549 cells migration together with reduced the intensity of phalloidin-rhodamine which detect filopodia and lamellipodia protrusions at 48 h of treatment. The protein expression indicated that fucoidan significantly suppressed the phosphorylation of focal adhesion kinase (FAK), Src, and extracellular signal-related kinase (ERK). In addition, the phosphorylation of p38 in A549 cells was found to be increased. CONCLUSIONS: Our data conclude that fucoidan exhibits anti-migratory activities against lung cancer A549 cells mediated by inhibiting ERK1/2 and FAK-Src pathway.

• ALGAE
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• v.22 no.3
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• pp.247-252
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• 2007

Crude fucoidan was extracted from the sporophyll of Korean Undaria pinnatifida collected at a coastal area ofWando, Korea, mainly by dilute acid extraction, ethanol precipitation, CaCU Precipitation, with an yield of approxi-mately 3.9% in mass. It was further purified by DEAE-cellulose column chromatography and its chemical composi-don and in vitro anticoagulant activity was determined. The average molecular mass of the purified fucoidan wasestimated about 2.1 x 103 kDa by size-fractionation HPLC and it consisted of neutral sugar (52.34% in mass), uronicacid (26.2%), and sulfate esters (7.4%). From the HPAEC-PAD analysis, the monosaccharide composition of thepurified fucoidan was shown to be fucose, galactose, xylose, and mannose, with a molar ratio of 1, 0.2, 0.02, 0.15,respectively, demonstrating that major monosacd-iande was fucose (72.3% in mol percentage) and other sugars,xylose (1.5%), galactose (14.6%), and mannose (10.9%) were present as minor component. The results suggested thatthis fucoidan is a sulfated, U-type fucoidan. The activated partial thrombloplastin time (APTT) assay of the purifiedfucoidan showed that the purified fucoidan elicited anticoagulant activity in a dose-dependent manner. Five jUg ofsporophyll fucoidan delayed the blood clotting time up to 5 times than untreated control and also up to 1.5 timesthan the same amount of the commercial fucoidan, respectively. Although it is preliminary, these results suggestthat the fucoidan of Korean Undaria vinnatifida sporophyll would be promising candidates for the development ofan anticoaeulant.

• Journal of Marine Bioscience and Biotechnology
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• v.9 no.1
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• pp.1-7
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• 2017

Perfluorooctane sulfonate (PFOS) is one of the most widely distributed environmental pollutants and causes neurotoxicities. Fucoidan is a main bioactive constituent of the brown sea-weed and has many functions in a variety of physiological conditions. The present study attempted to investigate the potential role of fucoidan as neuroprotective marine polypeptide in environmental pollutant-induced apoptosis of neuronal cells in culture. MTT assay showed that cell viability was significantly reduced to 68 % at $30{\mu}M$ PFOS, which was recovered up to 77% and 92% in the presence of fucoidan 25 and $50{\mu}g/ml$, respectively. Cytotoxicity assay showed that LDH release was significantly increased to 160% at $30{\mu}M$ PFOS but was reduced to 150% and 122% in the presence of fucoidan 25 and $50{\mu}g/ml$, respectively. Caspase-3 activity, a hallmark of apoptosis, was measured to determine the cytotoxicity of PFOS and the cytoprotective effects of fucoidan. PFOS induced a 250% increase of caspase-3 activity at $30{\mu}M$ but the increase was dampened to 180% and 130% in the presence of fucoidan 25 and $50{\mu}g/ml$, respectively. PFOS $30{\mu}M$ induced 180 % increase in ROS accumulation, which was effectively blocked by $50{\mu}g/ml$ fucoidan (120% of control). Our results demonstrated that PFOS is a powerful neurotoxicant and fucoidan may be a protective marine bioactive polypeptide against the neurotoxic environmental pollutants. It may contribute to establishing the potential role of fucoidan as a neuroprotective polypeptide that prevents the risk of neurological disorders from the possible neurotoxic pollutants.

• Preventive Nutrition and Food Science
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• v.13 no.4
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• pp.259-265
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• 2008

This study was designed to investigate the protective effect of fucoidan against AAPH-induced oxidative stress in LLC-PK1 cells (porcine kidney epithelial cells). Oxidative stress was induced by exposing of LLC-PK1 cells to the 1 mM 2,2'-azobis(2-amidino propane) dihydrochloride (AAPH) for 24 hr. Exposure of LLC-PK1 cells to 1 mM AAPH for 24 hr resulted in a significant (p<0.05) decrease in cell viability, but fucoidan treatment protected LLC-PK1 cells from AAPH-induced cell damage in a dose dependant manner. To investigate the protective action of fucoidan against AAPH-induced damage of LLC-PK1 cells, we measured the effects of fucoidan on lipid peroxidation and antioxidant enzymes activities of AAPH treated cells as well as scavenging activities on superoxide anion radical and hydroxyl radical. Fucoidan had protective effect against the AAPH-induced LLC-PK1 cellular damage and decreased lipid peroxidation and increased activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). Furthermore, fucoidan showed strong scavenging activity against superoxide anion radical. The $IC_{50}$ value of fucoidan was $48.37{\pm}1.54\;{\mu}g/mL$ for superoxide anion radical scavenging activity. The fucoidan also had high hydroxyl radical scavenging activity ($IC_{50}=32.03\;{\mu}g/mL$). These results indicate that fucoidan protects against AAPH-induced LLC-PK1 cell damage by inhibiting lipid peroxidation, increasing antioxidant enzyme activities and scavenging offree radicals.

• Macromolecular Research
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• v.17 no.2
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• pp.128-132
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• 2009

Fucoidan, a sulfated polysaccharide derived from brown seaweed, is an important material valued for its various biological functions, including anti-coagulation, anti-aging, and immune system support. In this study, we examined the potential of fucoidan as a novel emulsifying agent in BSA (bovine serum albumin)-stabilized emulsion at a neutral pH. We measured the dispersed oil-droplet size, surface zeta-potential and creaming formation of 0.5 wt% BSA emulsion (20 wt% oil traction) in the absence and presence of fucoidan. The average particle size and zeta-potential value were 625.4 nm and -30.91 mV in only BSA-stabilized emulsion and 745.2 nm and -44.2 mV in 1.0 wt% fucoidan-added BSA emulsion, respectively. This result suggested that some positive charges of the BSA molecules interacted with the negative charges of fucoidan to inhibit the flocculation among the oil droplets. The creaming rate calculated from the backscattering data measured by Turbiscan dramatically decreased in 1.0 wt% fucoidan-added BSA emulsion during storage. Accordingly, the repulsion forces induced among the oil particles coated with 1.0 wt% fucoidan in emulsion solution resulted in significantly increased emulsion stability. The turbidity of the BSA-stabilized emulsion at 500 nm decreased during five days of storage. However, the fucoidan-added BSA emulsion exhibited a higher value of turbidity than the BSA-stabilized emulsion did. In conclusion, an anionic sulfated fucoidan lowered the surface zeta-potential of BSA-coated oil droplets via the electrostatic interaction, and subsequently inhibited the flocculation among the oil droplets, thereby clearly minimizing the creaming and phase separation of the emulsion.

• Korean Chemical Engineering Research
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• v.49 no.6
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• pp.704-709
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• 2011

Depolymerization of fucoidan induced by contact glow discharge electrolysis(CGDE) was investigated. To utilize fucoidan as a functional food material after CGDE, organic acids were used as a electrolyte in CGDE process. Experimental results showed that CGDE using organic acid reduced the molecular weight of fucoidan effectively. As electrolyte concentration increased, onset voltage of glow discharge decreased and onset current of glow discharge increased. From the variation of molecular weight of fucoidan with the reaction time, it was demonstrated that the degradation of fucoidan followed a first-order rate law. Molecular weight of fucoidan treated with CGDE using organic acid was about 77 times lower compared to initial fucoidan with little free sulfate.

• Journal of Veterinary Clinics
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• v.34 no.2
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• pp.70-75
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• 2017

Fucoidan increases the chemotactic activity of peripheral blood polymorphonuclear cells (PMNs) through interleukin (IL)-8 produced by peripheral blood mononuclear cells (PBMCs). It has been demonstrated that fucoidan can regulate the chemotaxis of PMNs by activating F-actin polymerization. The objectives of this study are to investigate the direct effect of fucoidan on the chemotaxis of porcine PMNs and to examine whether this effect is associated with changes in phosphoinositide 3-kinase (PI3K) activity. The chemotactic activity of porcine PMNs was evaluated by modified Boyden chamber assay. Akt phosphorylation activity, a main downstream of PI3K, was measured by Western blotting assay. Fucoidan itself has no chemoattractant effect for PMNs. However, direct treatment of PMNs with fucoidan showed higher chemotactic activity to porcine recombinant (pr) IL-8 than that of PMNs without fucoidan. The increased chemotactic activity of fucoidan-treated PMNs to pr IL-8 was suppressed by treatment of wortmannin, an inhibitor of PI3K. Treatment of PMNs with fucoidan also increased Akt phosphorylation level. This increase was also suppressed by wortmannin. These results suggested that fucoidan can upregulate chemotactic activity of porcine PMNs to IL-8, which is associated with PI3K activation.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.272-278
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• 2017

Fucoidan has been reported to exhibit various beneficial activities ranging from to antivirus and anticancer properties. However, little information is available about the effects of fucoidan on cerebral ischemia-reperfusion injury (IRI). Our study aimed to explore the effects of fucoidan on cerebral IRI, as well as the underlying mechanisms. Sprague-Dawley (SD) rats were randomly subjected to four groups: Sham, IRI+saline (IRI+S), IRI+80 mg/kg fucoidan (IRI+F80), and IRI+160 mg/kg fucoidan (IRI+F160). Fucoidan (80 mg/kg or 160 mg/kg) was intraperitoneally injected from 7 days before the rats were induced to cerebral IRI model with middle cerebral artery occlusion (MCAO) method. At 24 h after reperfusion, neurological deficits and the total infarct volume were determined. The levels of inflammation-associated cytokines (interleukin (IL)-$1{\beta}$, IL-6, myeloperoxidase (MPO), and tumor necrosis factor (TNF)-${\alpha}$), oxidative stress-related proteins (malondialdehyde (MDA) and superoxide dismutase (SOD)) in the ischemic brain were measured by enzyme-linked immunosorbent assay (ELISA). Besides, the levels of apoptosis-related proteins (p-53, Bax, and B-cell lymphoma (Bcl)-2) and mitogen-activated protein kinase (MAPK) pathway (phosphorylation-extracellular signal-regulated kinase (p-ERK), p-c-Jun N-terminal kinase (JNK), and p-p38) were measured. Results showed that administration of fucoidan significantly reduced the neurological deficits and infarct volume compared to the IRI+S group in a dose-dependent manner. Also, fucoidan statistically decreased the levels of inflammation-associated cytokines, and oxidative stress-related proteins, inhibited apoptosis, and suppressed the MAPK pathway. So, Fucoidan plays a protective role in cerebral IRI might be by inhibition of MAPK pathway.