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Astaxanthin mediates inflammatory biomarkers associated with arthritis in human chondrosarcoma cells induced with interleukin‐1β
Author(s) -
Kimble Lindsey,
Mathison Bridget,
Chew Boon P
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.638.6
Subject(s) - astaxanthin , oxidative stress , reactive oxygen species , chemistry , chondrocyte , inflammation , antioxidant , arthritis , glutathione peroxidase , ebselen , glutathione , matrix metalloproteinase , downregulation and upregulation , immunology , biochemistry , medicine , superoxide dismutase , enzyme , in vitro , gene , carotenoid
Arthritis is characterized by chondrocyte dysfunction resulting in inflammation, matrix metalloproteinase (MMP) production and progressive degeneration of articular cartilage. Astaxanthin, a potent antioxidant, may downregulate inflammation‐associated factors involved in arthritis. We studied the uptake and protective effects of astaxanthin against chondrocyte dysfunction using SW‐1353 human chondrosarcoma cells. Cells were pre‐incubated with 0, 0.01, 0.1, or 1.0 μmol/L astaxanthin for 48 h, and oxidative stress induced with 10 ng/mL IL‐1β overnight. Astaxanthin (1.0 μmol/L) accumulated in SW‐1353 cells in a time‐dependent manner. IL‐1β alone suppressed intracellular antioxidant activity, resulting in overproduction of reactive oxygen species (ROS), MMP‐13, inflammatory cytokines and mediators. In contrast, pre‐incubation with astaxanthin increased ( P < 0.05) glutathione peroxidase activity and decreased ( P < 0.05) ROS, MMP‐13, IL‐6, TNF‐α and inflammatory mediators. Pre‐treatment with astaxanthin also downregulated transcriptional activation of NF‐κB and activator protein‐1, which play critical roles in downstream production of MMP, inflammatory cytokines and mediators. Astaxanthin protects against degenerative factors upregulated by IL‐1β, likely by scavenging ROS required for transcriptional activation. Supported by Washington State University.