Reduction of Oxidative Stress by Astaxanthin in Lipopolysaccharide-treated Human Gingival Fibroblasts

Objectives: Carotenoid Astaxanthin (AST), a potent antioxidant, has been thought to provide health benefits by decreasing the risk of oxidative stress-related diseases. However, the molecular mechanism is still not well understood. In this study, we report AST could prevent oxidation in human gingival fibroblasts　(HGFs).
Methods: HGFs were cultured with Porphyromonas gingivalis lipopolysaccharide (Pg LPS), AST and their combinations. After 24 h, the cell viability was measured by MTT assay. The intracellular Nitric oxide (NO) levels were detected with the NO-specific probe 4,5-diaminofluorescein-2/diacetate (DAF-2/DA), by fluorescence microscopy. Heme oxygenase -1 (HO-1) was detected by the Human Apoptosis Array.
Results: The proliferation rate of HGFs was dose-dependently decreased with Pg LPS alone by MTT assay. However, treatment with AST alone, or Pg LPS　and AST for 24 h did not affect the cell viability . AST suppressed PgLPS-induced NO production　via the inhibition of p38 MAPK. In contrast, AST induced the antioxidant enzyme, HO-1 .
Conclusions: These results suggest that AST decreased NO production by inhibition of p38 phosphorylation and its activation via the generation of　HO-1. AST may be useful to improve gingival inflammation in periodontal disease.