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        Fucoidan from <i>Undaria pinnatifida</i> regulates type II collagen and COX-2 expression via MAPK and PI3K pathways in rabbit articular chondrocytes

        Phull, Abdul Rehman,Kim, Song Ja VYDAVATELSTVO SLOVAK ACADEMIC PRESS - BRATISLAVA 2017 Biologia Vol.72 No.11

        <P><B>Abstract</B></P><P>Fucoidan is a sulfated polysaccharide widely distributed in brown seaweed. It exhibits several bioactivities, such as anti-cancer, anti-tumor, anti-microbial, anti-diabetic and anti-oxidant properties. However, the effects of fucoidan in chondrocytes are not well established. Previously, we have reported<I>in vitro</I>and<I>in vivo</I>anti-inflammatory effects of fucoidan. In this study, we evaluated the effects and regulatory mechanism of fucoidan derived from<I>Undaria pinnatifida</I>on the cyclooxygenase-2 (COX-2) and type II collagen in rabbit articular chondrocytes. Using western blotting and alcian blue staining, respectively, fucoidan was shown to induce type II collagen and sulfated proteoglycan in a dose- and time-dependent manner. Moreover, fucoidan inhibited the COX-2 expression in a dose- and time-dependent manner and increased the phosphorylation of extracellular signal-regulated kinase (ERK), p38, and AKT kinases in chondrocytes. The inhibition of p38 and AKT using SB203580 and LY294002, respectively, in the presence of fucoidan decreased the expression of type II collagen. However, ERK inhibition using PD98050 stimulated type II collagen expression. Fucoidan increased COX-2 expression in the presence of inhibitors of ERK, p38, and AKT kinases. These results conclusively suggested that fucoidan regulated type II collagen expression via the p38 and AKT pathways, and COX-2 expression via the p38, ERK and AKT pathways in rabbit articular chondrocytes. Moreover, given its ability to mediate cell differentiation and exert anti-inflammatory activity, fucoidan may represent a potential therapeutic substance for use in inflammatory conditions, including arthritis.</P>

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