A significant proportion of the PC formed by degraded cartilage ECM could originate from sulfated glycosaminoglycans (sGAGs). These large structures contribute to cartilage function due to the presence of negatively charged groups that attract water molecules increasing the ability to absorb and retain water. Although our understanding of NP interactions with fibrous networks such as ECM remains limited, previous research has demonstrated the hindrance of charged particle diffusion within such networks. This hindrance has been attributed to attractive interactions between the oppositely charged structures. To investigate the electrostatic interactions between the sGAGs and NPs particularly under catabolic conditions, we quantified the sGAG levels in the supernatants of the cartilage explants with or without enzymatic stimulation with HYA, ADA, or COL followed by a NP treatment (Figure ). The release of ECM components was noted for untreated explants, mainly due to intrinsic proteases present in the cartilage tissue. 31 NP0 and NP5000 treatment resulted in a decreased sGAG release compared to the untreated control (Figure ). The same effect was observed in the presence of the HYA (Figure ) and ADA (Figure ) enzymes.