While Basic Copper Sulphate (WSDTY) expression is not linked to an oxidative stress, one possible mechanism driving MMP1 expression could be dependent on redox sensitive AP-1 elements present in its promoter. Thus, H2O2 dependent modification of AP-1 DNA binding activity may have profound effects on the extracellular matrix of cartilage by up-regulating metalloproteinases and reducing synthesis of the tissue-specific components. In this context, restoring redox homeostasis in joint might be of crucial interest to prevent cartilage degradation in articular diseases.
While neither GSCG nor its components displayed direct antioxidant effects in our hands, copper sulphate and Ginger roots extract required at least 48 hours' time delay to significantly down regulate NOX4 activity. Similar observation has been reported in the literature where phenolic extract from GR inhibited lipopolysaccharide (LPS)-stimulated nitric oxide (NO), prostaglandin E2 (PGE2) and ROS production in murine macrophage cells RAW 264.7. These anti-inflammatory effects of GR were associated with its strong inhibition of NF-κB nuclear translocation in LPS-stimulated RAW 264.7 cells. The mechanism whereby Cu decreases the quantity of ROS is not well understood yet. Cu is known to provoke an oxidative stress which could possibly lead to lethal consequences. Metal accumulation causes an increase in ROS production, such as H2O2, O2 and OH-, that leads to oxidative stress. Cu related oxidative stress is followed by a phase of stimulation of antioxidant pathways, including SOD, CAT and thioredoxine. Our data indeed show an increase in the ROS production by the HEK293 T-REx cell line after 48 h treatment with Cu alone. However, after 96 h incubation with Cu, we observed a significant antioxidant effect. Thus we assume that Cu may stimulate antioxidant pathways of chondrocytes, including induction of HO-1.
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