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Sufficient levels of glutathione must be maintained to exert protective and biosynthetic functions ( 2 O 2 -induced oxidation ( FIGURE 2 The role of oxidative stress in articular cartilage degeneration Biochemical analysis of degenerative cartilage from patients with OA showed that there was a pathological relationship between the downregulation of SOD2 and cartilage degeneration in the progression of OA, suggesting that the redox balance centred on SOD2 in mitochondria plays a central role in the pathogenesis of KOA ( in vivo promotes the production of O 2 in mitochondria of chondrocytes, and the expression of SOD1 and SOD2 in mitochondria decreases, while mitochondrial dysfunction induced by superoxide in mitochondria will further lead to cartilage degeneration (Figure 3) Some studies have shown that Nox is involved in macrophage phagocytosis and neutrophil bactericidal activity, so Nox has a firmly established importance in immune function ( 2 and H 2 O 2 produced by Noxs in many cell types are essential for normal signal transduction of growth factors and cytokines ( 2 and H 2 O 2 ( FIGURE 3 NO in cartilage and synovium is produced by iNOS, which mediates the expression of inflammatory factors, inhibits the synthesis of collagen and proteoglycan, and induces chondrocyte apoptosis and pain ( One study found that NO alone did not result in chondrocyte death but that NO triggered apoptosis when it reacted with O 2 - to produce chondrocytes ( 2 reacts with NO to produce ONOO

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