It has been suggested that glucosamine may also have an anti-inflammatory action (Hua et al 2002). Glucosamine, but not N-acetyl glucosamine, inhibited human Glucosamine 598
neutrophil functions such as superoxide generation, phagocytosis, granule enzyme
release and chemotaxls In vitro (Hua et al 2002), and it has been shown that glucosamine and N-acetyl glucosamine both inhibit IL-1 -beta- and TNF-alpha-induced NO production in normal human articular chondrocytes (Shikhman et al 2001). Glucosamine has been also found to restore proteoglycan synthesis and prevent the production of inflammatory mediators induced by the cytokine IL-1 -beta in rat-articular chondrocytes in vitro (Gouze et al 2001). Furthermore, glucosamine has been found to suppress PGE2 production and partly suppress NO production in chondrocytes in vitro (Mello et al 2004, Nakamura et al 2004), as well as suppressing the production of matrix metalloproteases in normal chondrocytes and synoviocytes (Nakamura etal 2004).
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