Sulfated glucosamine inhibits oxidation of biomolecules in cells via a mechanism involving intracellular free radical scavenging

Abstract

Although, several effects of glucosamine and its sulfated form (sulfated glucosamine) have been proposed for the suppression of osteoarthritis, their exact mechanisms have not been completely elucidated. This study explains the novel possibility of involvement of sulfated glucosamine in improving cellular antioxidant potential and thereby controlling oxidative damage that could be effective for its therapeutic potential in osteoarthritis. Treatment with sulfated glucosamine to human chondrocytes and macrophages inhibited radical simulated oxidation of membrane lipids, proteins and DNA in a dose-dependent manner. Moreover, detection of reactive oxygen species by electron spin resonance (ESR) spectroscopy and 2',7'-dichlorodihydrofluororescein diacetate (DCFH-DA) fluorescence probe clearly confirmed effective radical scavenging potential of sulfated glucosamine in cellular and non-cellular systems. More importantly, NF-kappaB reporter gene assay and western blot analysis revealed that sulfated glucosamine inhibits radical mediated expression and activation of nuclear factor kappaB (NF-kappaB) proteins (transcription factor involves in expression of a number of genes related to osteoarthritis). Further, sulfated glucosamine enhanced reduced glutathione (GSH) level in oxidatively stressed human chondrocytes improving cellular redox balance. In conclusion, it is suggested that potential effects of sulfated glucosamine in controlling osteoarthritis might be partly via mechanisms involving direct scavenging of cellular radical species and alteration of oxidation mediated destructive events.