Lutein and β-Cryptoxanthin Inhibit Inflammatory Mediators in Human Chondrosarcoma Cells Induced with IL-1β

You are here:
< All Topics

Publication:

Open Nutrition Journal (2012), 6, 41-47

http://www.dissertations.wsu.edu/Thesis/Fall2009/M_Di-Filippo_100909.pdf

Author(s):

Michael M. Di Filippo, Bridget D. Mathison, Jean Soon Park and Boon P. Chewoileau, Judge, and David Bellar

Quansys Products Used:

 

Abstract:

Osteoarthritis (OA) and rheumatoid arthritis (RA) are characterized by the activation of
matrix-degrading proteinases and production of inflammatory cytokines and mediators by
chondrocytes in articular cartilage. Several studies have shown that the carotenoids lutein (Lu)
and β-cryptoxanthin (βCr) may be useful in downregulating factors involved in the progression
of OA and RA Therefore, the possible protective effects of Lu and βCr against arthritis were
studied using SW-1353 cells induced by interleukin-1β (IL-1β). Cells were cultured for 24 hr
with 0, 0.01, 0.1 and 1.0 µmol/L of Lu (Experiment 1) or βCr (Experiment 2) and stressed by IL1β for 24 hr. Conditioned medium was analyzed for proteinases, inflammatory cytokines and
mediators, and nuclear extract for NFκB. The addition of βCr had no effect on matrixmetalloproteinase-13 (MMP-13) production; however, 1.0 µmol/L Lu decreased matrix MMP-13
(P<0.02) and PGE2 (P<0.04) production. Similarly the addition of 0.1 and 0.01 µmol/L βCr also
decreased (P<0.01) PGE2 production. At various concentrations (0.01, 0.1, and 1.0 µmol/L), βCr
decreased the pro-inflammatory cytokines IL-1α (P<0.05), IL-2 (P<0.04), and IFN-γ. In contrast,
Lu increased the IL-1α, IL-2 (P<0.01), and interferon (IFN)-γ. Lu increased the antiinflammatory cytokines IL-4 (P<0.02) and IL-10, while βCr decreased IL-4 and IL-10 (P<0.02).
v
NFκB p50 was decreased by Lu at all concentrations tested including a 39% reduction in cultures
containing 0.1 µmol/L. The βCr also decreased concentrations of nuclear p50 by 38% in cells
preincubated with 1.0 µmol/L. In conclusion, Lu and βCr protected against degenerative factors
upregulated by IL-1β-stimulation, likely by scavenging reactive oxygen species required for
NFκB activation. Chondrocytes cultured in the presence of Lu downregulated factors involved in
cartilage destruction (MMP-13 and PGE2) and upregulated factors (IL-4) involved in tissueprotection, while addition of βCr resulted in strong downregulation of factors associated with
pro-inflammatory response (IL-1α, IL-2, and IFN-γ) and cartilage destruction (PGE2).

Next Urban Particulate matter activates Akt in human lung cells