β‐Cryptoxanthin and lutein mediate inflammatory mediators and cytokines in human chondrosarcoma cells induced with interleukin‐1β

Abstract

Arthritis is characterized by chondrocyte dysfunction resulting in inflammation, matrix metalloproteinase (MMP) production and the progressive degeneration of articular cartilage. β‐Cryptoxanthin (β‐Cr) and lutein (Lu) may downregulate inflammation‐associated factors involved in arthritis. We studied the uptake and protective effects of β‐Cr and Lu, alone and in combination, against chondrocyte dysfunction using SW‐1353 human chondrosarcoma cells induced with IL‐1β. β‐Cr and Lu (10 μmol/L) accumulated in SW‐1353 cells in a time‐dependent manner; β‐Cr and Lu in combination inhibited β‐Cr uptake. Cells were pre‐incubated with 0, 0.01, 0.1, or 1.0 μmol/L β‐Cr, Lu, or a mixture of β‐Cr and Lu for 48 h, then oxidative stress‐induced with 10 ng/mL IL‐1β overnight. Both β‐Cr and Lu, alone and in combination, increased (p<0.05) glutathione peroxidase activity. β‐Cr alone (0.1 μmol/L) decreased (p<0.05) MMP‐13, TNF‐α, inflammatory mediator production and NFκB translocation at the expense of IL‐2 and IFN‐γ upregulation. Lu alone decreased (p<0.05) TNF‐α, inflammatory mediators and NFκB, but did not downregulate MMP‐13. In combination, β‐Cr and Lu decreased (p<0.05) MMP‐13, inflammatory mediators and NFκB without inflammatory cytokine upregulation. Therefore, β‐Cr and Lu protect against degenerative factors upregulated by IL‐1β, likely by scavenging reactive oxygen species required for NFκB activation.