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Studies have shown that lutein (Lu) and β-cryptoxanthin (βCr) may down-regulate factors involved
in inflammation associated with osteoarthritis and rheumatoid arthritis. We studied the possible protective effects of Lu
and βCr in vitro against human chondrocyte dysfunction using a human chondrosarcoma cell line.
SW-1353 human chondrosarcoma cells were cultured for 24 hr in supplemented medium containing 0, 0.01, 0.1
or 1.0 μmol/L of Lu or βCr and subsequently stressed for 24 hr in the presence of 10 μg/L IL-1β. The resulting conditioned
medium was analyzed for matrix-metalloproteinase-13 (MMP-13), cytokines (IL-1α, IL-2, IL-4, IL-10, IFN-γ , IL-
6, IL-8, and TNF-α), and PGE2. Nuclear extract from the harvested cells was analyzed for NFκB.
Lu (1.0 μmol/L; P<0.05) but not βCr decreased MMP-13. Both Lu (1.0 μmol/L; P<0.05) and βCr (0.1 and 0.01
μmol/L; P<0.01) inhibited PGE2 production. All concentrations of βCr suppressed (P<0.05) IL-1α, IL-2 and IFN-γ production
while Lu increased concentrations of these cytokines. Lu increased (P<0.05) while βCr decreased IL-4 and IL-10
concentrations. NFκB p50 production was suppressed (P<0.01) by both Lu and βCr, with Lu being more inhibitory.
Therefore, Lu and βCr protected against IL-1β-induced chondrocyte dysfunction by down-regulating NFκB
activation and inhibiting inflammatory response, albeit through somewhat different pathways.