Substances tested

Stimulate matrix proteoglycan degradation and inhibit glycosaminoglycan synthesis in cartilage explants. The reference catabolic insult: most chondroprotective compounds in this table are tested against it.

Concentration-dependent suppression of IL-1 effects in cartilage organ culture. Inhibited binding of radiolabelled IL-1 alpha to rabbit articular chondrocytes and suppressed collagenase, gelatinase, stromelysin and prostanoid production by IL-1-activated chondrocytes.

Outperforms anakinra at joint retention and at preventing IL-1-induced cartilage inflammation. The problem it solves is residence time: anakinra clears the joint faster than the inflammation resolves.

Inhibits CLK2-mediated phosphorylation of SR splicing factors and DYRK1A-mediated phosphorylation of SIRT1 and FOXO1, modulating Wnt without touching beta-catenin. CLK2 inhibition induces early chondrogenesis; DYRK1A inhibition enhances mature chondrocyte function and carries the anti-inflammatory effect through NF-kB and STAT3. In the rat MIA model a single intra-articular injection increased joint cartilage, decreased pain and improved weight-bearing.

Promotes chondrocyte proliferation and extracellular matrix synthesis, increases cartilage thickness in a dose-dependent manner, and inhibits proteolytic enzyme activity. Reviewed as an effective DMOAD acting by both anti-catabolic and excitoanabolic routes.

Tested for whether adding sprifermin during storage preserves the depth-dependent mechanical inhomogeneity of articular cartilage, the property fresh allografts lose at 4 degrees C.

Two-sided. In injured cartilage and post-traumatic OA models it rescues matrix loss and chondrocyte viability. In healthy cartilage and isolated chondrocytes many studies report significant increases in apoptosis instead. Whether it protects or kills depends on dose, duration of exposure and the model used.

Attenuated IL-1beta-induced falls in ACAN, COL2A1 and SOX9 and reduced IL-1beta-induced MMP13, ADAMTS5, COL10A1, RUNX2 and IL-6. Lowered the ALK1/ALK5 protein ratio, reduced Smad1/5/9 phosphorylation and increased Smad2/3 phosphorylation. The authors state docking and mutagenesis did not demonstrate direct eugenol-ALK1 binding.

Alleviates inflammatory injury in osteoarthritis chondrocytes through ERBB2-coupled JAK2/STAT3 suppression, identified by network pharmacology and then tested experimentally.

In IL-1beta-stimulated ATDC5 chondrocytes it restored aggrecan and collagen II, suppressed MMP3 and MMP13, and cut reactive oxygen species, lipid peroxidation and intracellular Fe2+. Nrf2 silencing removed the antioxidant, matrix-preserving and anti-ferroptotic effects, which is the evidence that the effect runs through Nrf2. In the DMM mouse model it alleviated cartilage degeneration without overt organ toxicity.

Ameliorates ferroptosis-associated features and osteoarthritis progression. Cartilage assessed by safranin O and H and E staining; chondrocyte viability and apoptosis by CCK-8 and flow cytometry, with the mechanism mapped by network pharmacology.