ABSTRACT During the inflammatory processes, reactive oxygen species (ROS), namely superoxide radical (O2.-), singlet oxygen (1O2), hydrogen peroxide (H2O2), hydroxyl radical (HO.), and hypochlorous acid (HOCl) and nitrogen reactive species (NRS), namely nitric oxide (.NO), and peroxynitrite anion (ONOO-) are generally formed and have been implicated in its pathophysiology. These reactive species are responsible for many deleterious effects observed in several inflammatory processes, as is the case of inflammatory arthritis. One of the prominent features of inflammatory arthritis is the loss of viscosity of the synovial fluid due to the HO.- induced degradation of its major macromolecular component, hyaluronan. Noteworthy, ROS liberated from phagocyte cells through the inflammatory processes are implicated in the activation of nuclear factor κB (NF-κB), which induces the transcription of inflammatory cytokines and COX. Non-steroidal anti-inflammatory drugs (NSAIDs) exert anti-inflammtory, analgestic and antipyretic activities. Their mechanism of action is mainly due to the inhibition of prostaglandin and leukotriene synthesis, which is mediated by the COX and lipoxygenase enzymes, respectively. NSAIDs also inhibit activation of neutrophils. However, taking into account that ROS and RNS are also involved in the deleterious effects of inflammation, there has been a considerable interest in the possibility that these inhibitor effects of NSAIDs may be potentiated by an associated antioxidant activity of the drugs, or by a concomitant administration of other antioxidant compounds. This review gives an overview of the studies performed so far that point to the contribution of the antioxidant activity of the NSAIDs for the anti-inflammatory therapeutic outcome.
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